Analysis of transcriptomic data reveals the landscape of cholesterol metabolism in prostate cancer and impact of related signature on survival

Background Cholesterol metabolism is essential for the development and progression of prostate cancer (PCa). Our previous study provided a new insight of cholesterol metabolism in the systematic management of PCa. However, the comprehensive role of cholesterol metabolism in PCa remains unclear. Meth...

Full description

Saved in:
Bibliographic Details
Published inDiscover. Oncology Vol. 15; no. 1; pp. 777 - 24
Main Authors Sun, Jian-Xuan, An, Ye, Xu, Meng-Yao, Ma, Si-Yang, Liu, Chen-Qian, Xu, Jin-Zhou, Xia, Qi-Dong, Wang, Shao-Gang
Format Journal Article
LanguageEnglish
Published New York Springer US 18.12.2024
Springer Nature B.V
Springer
Subjects
Androgens
Cancer Research
Cancer therapies
Cell growth
Chemotherapy
Cholesterol
Cholesterol metabolism
Genes
Immunotherapy
Internal Medicine
Medical prognosis
Medicine
Medicine & Public Health
Metabolism
Molecular Medicine
Mortality
Oncology
Penicillin
Prostate cancer
Proteins
Radiation therapy
Radiotherapy
Statins
Surgical Oncology
Tumor microenvironment
Tumor mutation burden
United States > US
China
Chemotherapy
Tumor microenvironment
Cholesterol metabolism
Prostate cancer
Immunotherapy
Tumor mutation burden
Online AccessGet full text

Cover

Abstract Background Cholesterol metabolism is essential for the development and progression of prostate cancer (PCa). Our previous study provided a new insight of cholesterol metabolism in the systematic management of PCa. However, the comprehensive role of cholesterol metabolism in PCa remains unclear. Methods Using the cholesterol metabolism related genes (CMRGs) downloaded from the MSigDB database, and gene expression data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), we constructed a cholesterol risk index by the least absolute shrinkage and selection operator (LASSO) model, and correlated the risk index with prognosis, tumor mutation burden (TMB), tumor microenvironment (TME) infiltration and response to chemotherapy and immunotherapy. RT-qPCR, western blot, immunohistochemistry, cell proliferation assays by CCK-8 and EdU assays, and cell apoptosis assays by flow cytometry analysis were also performed. Results We found PCa was tightly correlated with the cholesterol metabolism pathways. The cholesterol risk index was an excellent and independent predictor of prognosis for PCa. A nomogram involving the risk index and other clinical factors (age, T stage) was established to explore the clinical value of risk index. We found high-risk index group was associated with worse prognosis, higher TMB, lower infiltration level of CD8 + T cells and a worse response to chemotherapy and immunotherapy. RT-qPCR, western blot and immunohistochemical staining validated the expression level of important CMRGs in PCa. In vitro experiments revealed downregulation of cholesterol metabolism could inhibit the proliferation of PCa cells and promoted their apoptosis. Conclusions We demonstrated the comprehensive role of cholesterol metabolism in PCa. Using the risk index, we could predict the prognosis, TME infiltration and response to chemotherapy/immunotherapy of PCa. Better understanding and evaluating the cholesterol metabolism could aid in precision medicine and promoting prognosis of PCa.
AbstractList Cholesterol metabolism is essential for the development and progression of prostate cancer (PCa). Our previous study provided a new insight of cholesterol metabolism in the systematic management of PCa. However, the comprehensive role of cholesterol metabolism in PCa remains unclear. Using the cholesterol metabolism related genes (CMRGs) downloaded from the MSigDB database, and gene expression data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), we constructed a cholesterol risk index by the least absolute shrinkage and selection operator (LASSO) model, and correlated the risk index with prognosis, tumor mutation burden (TMB), tumor microenvironment (TME) infiltration and response to chemotherapy and immunotherapy. RT-qPCR, western blot, immunohistochemistry, cell proliferation assays by CCK-8 and EdU assays, and cell apoptosis assays by flow cytometry analysis were also performed. We found PCa was tightly correlated with the cholesterol metabolism pathways. The cholesterol risk index was an excellent and independent predictor of prognosis for PCa. A nomogram involving the risk index and other clinical factors (age, T stage) was established to explore the clinical value of risk index. We found high-risk index group was associated with worse prognosis, higher TMB, lower infiltration level of CD8 T cells and a worse response to chemotherapy and immunotherapy. RT-qPCR, western blot and immunohistochemical staining validated the expression level of important CMRGs in PCa. In vitro experiments revealed downregulation of cholesterol metabolism could inhibit the proliferation of PCa cells and promoted their apoptosis. We demonstrated the comprehensive role of cholesterol metabolism in PCa. Using the risk index, we could predict the prognosis, TME infiltration and response to chemotherapy/immunotherapy of PCa. Better understanding and evaluating the cholesterol metabolism could aid in precision medicine and promoting prognosis of PCa.
Cholesterol metabolism is essential for the development and progression of prostate cancer (PCa). Our previous study provided a new insight of cholesterol metabolism in the systematic management of PCa. However, the comprehensive role of cholesterol metabolism in PCa remains unclear.BACKGROUNDCholesterol metabolism is essential for the development and progression of prostate cancer (PCa). Our previous study provided a new insight of cholesterol metabolism in the systematic management of PCa. However, the comprehensive role of cholesterol metabolism in PCa remains unclear.Using the cholesterol metabolism related genes (CMRGs) downloaded from the MSigDB database, and gene expression data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), we constructed a cholesterol risk index by the least absolute shrinkage and selection operator (LASSO) model, and correlated the risk index with prognosis, tumor mutation burden (TMB), tumor microenvironment (TME) infiltration and response to chemotherapy and immunotherapy. RT-qPCR, western blot, immunohistochemistry, cell proliferation assays by CCK-8 and EdU assays, and cell apoptosis assays by flow cytometry analysis were also performed.METHODSUsing the cholesterol metabolism related genes (CMRGs) downloaded from the MSigDB database, and gene expression data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), we constructed a cholesterol risk index by the least absolute shrinkage and selection operator (LASSO) model, and correlated the risk index with prognosis, tumor mutation burden (TMB), tumor microenvironment (TME) infiltration and response to chemotherapy and immunotherapy. RT-qPCR, western blot, immunohistochemistry, cell proliferation assays by CCK-8 and EdU assays, and cell apoptosis assays by flow cytometry analysis were also performed.We found PCa was tightly correlated with the cholesterol metabolism pathways. The cholesterol risk index was an excellent and independent predictor of prognosis for PCa. A nomogram involving the risk index and other clinical factors (age, T stage) was established to explore the clinical value of risk index. We found high-risk index group was associated with worse prognosis, higher TMB, lower infiltration level of CD8+ T cells and a worse response to chemotherapy and immunotherapy. RT-qPCR, western blot and immunohistochemical staining validated the expression level of important CMRGs in PCa. In vitro experiments revealed downregulation of cholesterol metabolism could inhibit the proliferation of PCa cells and promoted their apoptosis.RESULTSWe found PCa was tightly correlated with the cholesterol metabolism pathways. The cholesterol risk index was an excellent and independent predictor of prognosis for PCa. A nomogram involving the risk index and other clinical factors (age, T stage) was established to explore the clinical value of risk index. We found high-risk index group was associated with worse prognosis, higher TMB, lower infiltration level of CD8+ T cells and a worse response to chemotherapy and immunotherapy. RT-qPCR, western blot and immunohistochemical staining validated the expression level of important CMRGs in PCa. In vitro experiments revealed downregulation of cholesterol metabolism could inhibit the proliferation of PCa cells and promoted their apoptosis.We demonstrated the comprehensive role of cholesterol metabolism in PCa. Using the risk index, we could predict the prognosis, TME infiltration and response to chemotherapy/immunotherapy of PCa. Better understanding and evaluating the cholesterol metabolism could aid in precision medicine and promoting prognosis of PCa.CONCLUSIONSWe demonstrated the comprehensive role of cholesterol metabolism in PCa. Using the risk index, we could predict the prognosis, TME infiltration and response to chemotherapy/immunotherapy of PCa. Better understanding and evaluating the cholesterol metabolism could aid in precision medicine and promoting prognosis of PCa.
Abstract Background Cholesterol metabolism is essential for the development and progression of prostate cancer (PCa). Our previous study provided a new insight of cholesterol metabolism in the systematic management of PCa. However, the comprehensive role of cholesterol metabolism in PCa remains unclear. Methods Using the cholesterol metabolism related genes (CMRGs) downloaded from the MSigDB database, and gene expression data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), we constructed a cholesterol risk index by the least absolute shrinkage and selection operator (LASSO) model, and correlated the risk index with prognosis, tumor mutation burden (TMB), tumor microenvironment (TME) infiltration and response to chemotherapy and immunotherapy. RT-qPCR, western blot, immunohistochemistry, cell proliferation assays by CCK-8 and EdU assays, and cell apoptosis assays by flow cytometry analysis were also performed. Results We found PCa was tightly correlated with the cholesterol metabolism pathways. The cholesterol risk index was an excellent and independent predictor of prognosis for PCa. A nomogram involving the risk index and other clinical factors (age, T stage) was established to explore the clinical value of risk index. We found high-risk index group was associated with worse prognosis, higher TMB, lower infiltration level of CD8+ T cells and a worse response to chemotherapy and immunotherapy. RT-qPCR, western blot and immunohistochemical staining validated the expression level of important CMRGs in PCa. In vitro experiments revealed downregulation of cholesterol metabolism could inhibit the proliferation of PCa cells and promoted their apoptosis. Conclusions We demonstrated the comprehensive role of cholesterol metabolism in PCa. Using the risk index, we could predict the prognosis, TME infiltration and response to chemotherapy/immunotherapy of PCa. Better understanding and evaluating the cholesterol metabolism could aid in precision medicine and promoting prognosis of PCa.
Background Cholesterol metabolism is essential for the development and progression of prostate cancer (PCa). Our previous study provided a new insight of cholesterol metabolism in the systematic management of PCa. However, the comprehensive role of cholesterol metabolism in PCa remains unclear. Methods Using the cholesterol metabolism related genes (CMRGs) downloaded from the MSigDB database, and gene expression data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), we constructed a cholesterol risk index by the least absolute shrinkage and selection operator (LASSO) model, and correlated the risk index with prognosis, tumor mutation burden (TMB), tumor microenvironment (TME) infiltration and response to chemotherapy and immunotherapy. RT-qPCR, western blot, immunohistochemistry, cell proliferation assays by CCK-8 and EdU assays, and cell apoptosis assays by flow cytometry analysis were also performed. Results We found PCa was tightly correlated with the cholesterol metabolism pathways. The cholesterol risk index was an excellent and independent predictor of prognosis for PCa. A nomogram involving the risk index and other clinical factors (age, T stage) was established to explore the clinical value of risk index. We found high-risk index group was associated with worse prognosis, higher TMB, lower infiltration level of CD8 + T cells and a worse response to chemotherapy and immunotherapy. RT-qPCR, western blot and immunohistochemical staining validated the expression level of important CMRGs in PCa. In vitro experiments revealed downregulation of cholesterol metabolism could inhibit the proliferation of PCa cells and promoted their apoptosis. Conclusions We demonstrated the comprehensive role of cholesterol metabolism in PCa. Using the risk index, we could predict the prognosis, TME infiltration and response to chemotherapy/immunotherapy of PCa. Better understanding and evaluating the cholesterol metabolism could aid in precision medicine and promoting prognosis of PCa.
BackgroundCholesterol metabolism is essential for the development and progression of prostate cancer (PCa). Our previous study provided a new insight of cholesterol metabolism in the systematic management of PCa. However, the comprehensive role of cholesterol metabolism in PCa remains unclear.MethodsUsing the cholesterol metabolism related genes (CMRGs) downloaded from the MSigDB database, and gene expression data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), we constructed a cholesterol risk index by the least absolute shrinkage and selection operator (LASSO) model, and correlated the risk index with prognosis, tumor mutation burden (TMB), tumor microenvironment (TME) infiltration and response to chemotherapy and immunotherapy. RT-qPCR, western blot, immunohistochemistry, cell proliferation assays by CCK-8 and EdU assays, and cell apoptosis assays by flow cytometry analysis were also performed.ResultsWe found PCa was tightly correlated with the cholesterol metabolism pathways. The cholesterol risk index was an excellent and independent predictor of prognosis for PCa. A nomogram involving the risk index and other clinical factors (age, T stage) was established to explore the clinical value of risk index. We found high-risk index group was associated with worse prognosis, higher TMB, lower infiltration level of CD8+ T cells and a worse response to chemotherapy and immunotherapy. RT-qPCR, western blot and immunohistochemical staining validated the expression level of important CMRGs in PCa. In vitro experiments revealed downregulation of cholesterol metabolism could inhibit the proliferation of PCa cells and promoted their apoptosis.ConclusionsWe demonstrated the comprehensive role of cholesterol metabolism in PCa. Using the risk index, we could predict the prognosis, TME infiltration and response to chemotherapy/immunotherapy of PCa. Better understanding and evaluating the cholesterol metabolism could aid in precision medicine and promoting prognosis of PCa.
ArticleNumber 777
Author An, Ye
Xu, Jin-Zhou
Xu, Meng-Yao
Liu, Chen-Qian
Ma, Si-Yang
Wang, Shao-Gang
Sun, Jian-Xuan
Xia, Qi-Dong
Author_xml – sequence: 1
  givenname: Jian-Xuan
  surname: Sun
  fullname: Sun, Jian-Xuan
  organization: Department and Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 2
  givenname: Ye
  surname: An
  fullname: An, Ye
  organization: Department and Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 3
  givenname: Meng-Yao
  surname: Xu
  fullname: Xu, Meng-Yao
  organization: Department and Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 4
  givenname: Si-Yang
  surname: Ma
  fullname: Ma, Si-Yang
  organization: Department and Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 5
  givenname: Chen-Qian
  surname: Liu
  fullname: Liu, Chen-Qian
  organization: Department and Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Laboratory of Signaling and Gene Regulation, Cecil H. and Ida Green Center for Reproductive Biology Sciences, University of Texas Southwestern Medical Center
– sequence: 6
  givenname: Jin-Zhou
  surname: Xu
  fullname: Xu, Jin-Zhou
  organization: Department and Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 7
  givenname: Qi-Dong
  surname: Xia
  fullname: Xia, Qi-Dong
  email: qidongxia_md@163.com
  organization: Department and Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology
– sequence: 8
  givenname: Shao-Gang
  surname: Wang
  fullname: Wang, Shao-Gang
  email: sgwangtjm@163.com
  organization: Department and Institute of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology
BackLink https://www.ncbi.nlm.nih.gov/pubmed/39692951$$D View this record in MEDLINE/PubMed
BookMark eNp9ks9uFSEUxiemxv6xL-DCkLhxMwoMwwwr0zRqmzRxo2vCwJl7uWFgBOamfQmfWW6n1taFKwj8vu-cfOecVkc-eKiqNwR_IBh3HxOhvKM1pqzGhLd9ffuiOqFdg2uOCTl6cj-uzlPaYYxpS5oGt6-q40ZwQUVLTqpfF165u2QTCiPKUfmko51zmKxGRmWFIuxBuYTyFpBT3iStZjjAehscpAwxODRBVkNwNk3IejTHkLLKgLTyGiIqKmSnWel80EVw5c-gZDde5SUWM4_SEvd2r9zr6uVYqsH5w3lW_fjy-fvlVX3z7ev15cVNrZmgueYj64UmhhJoB80ZEYz2go2j4YJp0lDajrjEAtpohbXhHVDcGcZaYkaiRHNWXa--JqidnKOdVLyTQVl5_xDiRqqYrXYgR0NYUdKeKM4MHYRhSnDW93jgWI-meH1aveZlmMBo8CVH98z0-Y-3W7kJe0nK3DjGTXF4_-AQw8-lhConmzS4kjeEJcmGMC7ahnNW0Hf_oLuwxDLDleKs46Qr1NunLT328mfuBaAroMusUoTxESFYHvZLrvsly37J-_2St0XUrKJUYL-B-Lf2f1S_ARnv1XE
Cites_doi 10.1007/s12094-022-02857-0
10.1200/jco.19.01638
10.1371/journal.pone.0107468
10.1002/ijc.23928
10.1038/s41586-020-2135-x
10.1038/s41467-021-25325-9
10.1101/cshperspect.a001008
10.1016/j.pathol.2020.07
10.1016/j.eururo.2020.09.042
10.1016/j.euf.2019.06.004
10.1016/j.cell.2011.02.013
10.1016/j.canlet.2017.04.025
10.1158/1055-9965.Epi-14-1329
10.1007/s13238-020-00786-8
10.1016/j.intimp.2020.106709
10.1002/jcb.27646
10.1016/j.immuni.2018.03
10.1038/ng.2279
10.1038/nrurol.2016.199
10.1016/j.euo.2022.10.003
10.1089/omi.2011.0118
10.1007/s12094-012-0855-6
10.1186/s12929-018-0430-8
10.4161/cc.27767
10.1158/0008-5472.can-2148-2
10.1016/j.cmet.2014.01.019
10.3389/fimmu.2020.583084
10.1016/j.immuni.2019.01.020
10.1007/s10555-013-9470-4
10.3322/caac.21708
10.1016/j.celrep.2016.12.019
10.3892/mmr.2010.332
10.1016/j.cell.2017.08.028
10.1186/s13046-018-0851-y
10.1186/s12943-021-01452-1
10.1158/0008-5472.Can-16-0903
10.1093/nar/gkv007
10.1016/j.ccell.2016.05.004
10.1016/j.cmet.2019.04.002
10.1093/nar/gkaa407
10.1186/1471-2105-14-7
10.1038/s42255-020-0174-0
10.1038/s41388-021-01786-6
10.15252/embr.201439246
10.1016/j.ccell.2015.09.021
10.1093/bioinformatics/bts034
10.1186/s12885
10.4103/ijmr
10.1038/s41588-020-0664-8
10.1126/science.1260419
10.1038/ncb3427
10.1038/s41572-020-00243-0
10.1006/meth.2001.1262
10.3390/cancers13184696
10.1002/ijc.31817
10.3389/fonc.2022.887854
10.1210/endo-121-4-1461
10.1186/s10020-018-0035-4
10.1016/j.biomaterials.2017.06.013
10.1111/j.1464-410x.1997.tb00800.x
10.3322/caac.21660
10.1038/s41391-017-0030-9
10.3390/cancers14174293
10.3390/cells9122653
10.1093/annonc/mdy495
ContentType Journal Article
Copyright The Author(s) 2024
2024. The Author(s).
Copyright Springer Nature B.V. Dec 2024
The Author(s) 2024 2024
Copyright_xml – notice: The Author(s) 2024
– notice: 2024. The Author(s).
– notice: Copyright Springer Nature B.V. Dec 2024
– notice: The Author(s) 2024 2024
DBID C6C
AAYXX
CITATION
NPM
3V.
7RV
7X7
7XB
8FI
8FJ
8FK
ABUWG
AFKRA
AZQEC
BENPR
CCPQU
DWQXO
FYUFA
GHDGH
K9.
KB0
M0S
NAPCQ
PHGZM
PHGZT
PIMPY
PKEHL
PPXIY
PQEST
PQQKQ
PQUKI
PRINS
7X8
5PM
DOA
DOI 10.1007/s12672-024-01658-x
DatabaseName Springer Nature OA Free Journals
CrossRef
PubMed
ProQuest Central (Corporate)
Nursing & Allied Health Database
Health & Medical Collection
ProQuest Central (purchase pre-March 2016)
Hospital Premium Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Central (Alumni)
ProQuest Central UK/Ireland
ProQuest Central Essentials
ProQuest Central
ProQuest One Community College
ProQuest Central Korea
Health Research Premium Collection
Health Research Premium Collection (Alumni)
ProQuest Health & Medical Complete (Alumni)
Nursing & Allied Health Database (Alumni Edition)
Health & Medical Collection (Alumni)
Nursing & Allied Health Premium
ProQuest Central Premium
ProQuest One Academic
Publicly Available Content Database
ProQuest One Academic Middle East (New)
ProQuest One Health & Nursing
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Academic
ProQuest One Academic UKI Edition
ProQuest Central China
MEDLINE - Academic
PubMed Central (Full Participant titles)
DOAJ Directory of Open Access Journals
DatabaseTitle CrossRef
PubMed
Publicly Available Content Database
ProQuest One Academic Middle East (New)
ProQuest Central Essentials
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
ProQuest One Community College
ProQuest One Health & Nursing
ProQuest Central China
ProQuest Central
Health Research Premium Collection
Health and Medicine Complete (Alumni Edition)
ProQuest Central Korea
ProQuest Central (New)
ProQuest One Academic Eastern Edition
ProQuest Nursing & Allied Health Source
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
ProQuest Hospital Collection (Alumni)
Nursing & Allied Health Premium
ProQuest Health & Medical Complete
ProQuest One Academic UKI Edition
ProQuest Nursing & Allied Health Source (Alumni)
ProQuest One Academic
ProQuest One Academic (New)
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList PubMed
MEDLINE - Academic


Publicly Available Content Database
Database_xml – sequence: 1
  dbid: C6C
  name: Springer Nature OA Free Journals
  url: http://www.springeropen.com/
  sourceTypes: Publisher
– sequence: 2
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 3
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 4
  dbid: BENPR
  name: ProQuest Central
  url: https://www.proquest.com/central
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 2730-6011
EndPage 24
ExternalDocumentID oai_doaj_org_article_fd14d44281a64d2b9d4a964880b60cfd
PMC11656003
39692951
10_1007_s12672_024_01658_x
Genre Journal Article
GeographicLocations United States--US
China
GeographicLocations_xml – name: China
– name: United States--US
GrantInformation_xml – fundername: Undergraduate Training Program for Innovation and Entrepreneurship
  grantid: 202210487012
– fundername: National Natural Science Foundation of China
  grantid: 81772729
GroupedDBID 0R~
2JY
53G
7RV
7X7
8FI
8FJ
AAJSJ
AAYZJ
ABEEZ
ABUWG
AFBBN
AFKRA
ALIPV
ALMA_UNASSIGNED_HOLDINGS
BENPR
BGNMA
C6C
CCPQU
EBS
FYUFA
GROUPED_DOAJ
HMCUK
M4Y
NAPCQ
NU0
OK1
PGMZT
PIMPY
ROL
RPM
RSV
SOJ
UKHRP
AASML
AAYXX
CITATION
PHGZM
PHGZT
NPM
3V.
7XB
8FK
AZQEC
DWQXO
K9.
PKEHL
PPXIY
PQEST
PQQKQ
PQUKI
PRINS
7X8
5PM
PUEGO
ID FETCH-LOGICAL-c492t-6f489c1d21e5bc641942894ffd694c13225f0016ecdca0cd67e207d4451df1a93
IEDL.DBID C6C
ISSN 2730-6011
IngestDate Wed Aug 27 00:46:12 EDT 2025
Thu Aug 21 18:30:22 EDT 2025
Fri Jul 11 03:22:03 EDT 2025
Fri Jul 25 21:27:09 EDT 2025
Sun Mar 30 02:12:35 EDT 2025
Tue Jul 01 01:11:14 EDT 2025
Fri Feb 21 02:36:05 EST 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 1
Keywords Chemotherapy
Tumor microenvironment
Cholesterol metabolism
Prostate cancer
Immunotherapy
Tumor mutation burden
Language English
License 2024. The Author(s).
Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c492t-6f489c1d21e5bc641942894ffd694c13225f0016ecdca0cd67e207d4451df1a93
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
OpenAccessLink https://doi.org/10.1007/s12672-024-01658-x
PMID 39692951
PQID 3146647617
PQPubID 5642930
PageCount 24
ParticipantIDs doaj_primary_oai_doaj_org_article_fd14d44281a64d2b9d4a964880b60cfd
pubmedcentral_primary_oai_pubmedcentral_nih_gov_11656003
proquest_miscellaneous_3146953664
proquest_journals_3146647617
pubmed_primary_39692951
crossref_primary_10_1007_s12672_024_01658_x
springer_journals_10_1007_s12672_024_01658_x
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2024-12-18
PublicationDateYYYYMMDD 2024-12-18
PublicationDate_xml – month: 12
  year: 2024
  text: 2024-12-18
  day: 18
PublicationDecade 2020
PublicationPlace New York
PublicationPlace_xml – name: New York
– name: United States
PublicationTitle Discover. Oncology
PublicationTitleAbbrev Discov Onc
PublicationTitleAlternate Discov Oncol
PublicationYear 2024
Publisher Springer US
Springer Nature B.V
Springer
Publisher_xml – name: Springer US
– name: Springer Nature B.V
– name: Springer
References RJ Rebello (1658_CR33) 2021; 7
MA Alfaqih (1658_CR42) 2017; 14
L YuPeng (1658_CR12) 2015; 24
V Thorsson (1658_CR28) 2018; 48
JT Leek (1658_CR17) 2012; 28
Y Pan (1658_CR29) 2020; 11
A Amaro (1658_CR5) 2014; 33
S Ma (1658_CR50) 2018; 37
X Zheng (1658_CR48) 2021; 20
A Mandel (1658_CR46) 2018; 24
T Li (1658_CR19) 2020; 48
P Geeleher (1658_CR22) 2014; 9
G Singh (1658_CR36) 2017; 146
C Luo (1658_CR26) 2020; 86
G Yu (1658_CR21) 2012; 16
S Hao (1658_CR31) 2017; 140
A Brizzolara (1658_CR47) 2017; 400
C Kalogirou (1658_CR15) 2021; 12
AM Traish (1658_CR44) 1987; 121
P Charoentong (1658_CR23) 2017; 18
C Cheng (1658_CR38) 2015; 28
S Hänzelmann (1658_CR20) 2013; 14
TA Chan (1658_CR25) 2019; 30
CE Barbieri (1658_CR61) 2012; 44
KJ Livak (1658_CR16) 2001; 25
MW Pickup (1658_CR64) 2014; 15
SL Ettinger (1658_CR40) 2004; 64
KH Stopsack (1658_CR14) 2016; 76
X Ma (1658_CR65) 2019; 30
D Hanahan (1658_CR63) 2011; 144
H Sung (1658_CR1) 2021; 71
G Di Lorenzo (1658_CR45) 2002; 8
SH Tan (1658_CR56) 2021; 53
H Lilja (1658_CR4) 1997; 79
A Siltari (1658_CR11) 2022
M Teng (1658_CR59) 2021; 12
RL Siegel (1658_CR2) 2022; 72
J Hedegaard (1658_CR41) 2016; 30
L Mao (1658_CR52) 2021; 40
JX Sun (1658_CR7) 2022; 12
T Heir (1658_CR13) 2016; 16
B Huang (1658_CR39) 2020; 2
A Parrales (1658_CR66) 2016; 18
J Li (1658_CR62) 2020; 580
JB Wing (1658_CR32) 2019; 50
N Scaglia (1658_CR67) 2014; 13
MM Pomerantz (1658_CR60) 2020; 52
N Mottet (1658_CR3) 2021; 79
L Škara (1658_CR37) 2021
M Olivier (1658_CR58) 2010; 2
J Jamnagerwalla (1658_CR35) 2018; 21
T Van den Broeck (1658_CR6) 2020; 6
G Aurilio (1658_CR9) 2020
CP Schaffner (1658_CR10) 1981; 75a
S Yue (1658_CR43) 2014; 19
N Lobo (1658_CR8) 2022; 5
ER Kastenhuber (1658_CR57) 2017; 170
M Najafi (1658_CR30) 2019; 120
ES Antonarakis (1658_CR34) 2020; 38
T Ding (1658_CR54) 2010; 3
MC Sharma (1658_CR49) 2019; 144
CY Chen (1658_CR51) 2018; 25
M Uhlén (1658_CR24) 2015; 347
X Zhang (1658_CR53) 2012; 14
J Inokuchi (1658_CR55) 2009; 124
J Liao (1658_CR27) 2022; 24
ME Ritchie (1658_CR18) 2015; 43
References_xml – volume: 24
  start-page: 1986
  issue: 10
  year: 2022
  ident: 1658_CR27
  publication-title: Clin Transl Oncol
  doi: 10.1007/s12094-022-02857-0
– volume: 38
  start-page: 395
  issue: 5
  year: 2020
  ident: 1658_CR34
  publication-title: J Clin Oncol
  doi: 10.1200/jco.19.01638
– volume: 9
  start-page: e107468
  issue: 9
  year: 2014
  ident: 1658_CR22
  publication-title: PLoS ONE
  doi: 10.1371/journal.pone.0107468
– volume: 124
  start-page: 68
  issue: 1
  year: 2009
  ident: 1658_CR55
  publication-title: Int J Cancer
  doi: 10.1002/ijc.23928
– volume: 580
  start-page: 93
  issue: 7801
  year: 2020
  ident: 1658_CR62
  publication-title: Nature
  doi: 10.1038/s41586-020-2135-x
– volume: 12
  start-page: 5066
  issue: 1
  year: 2021
  ident: 1658_CR15
  publication-title: Nat Commun
  doi: 10.1038/s41467-021-25325-9
– volume: 2
  start-page: a001008
  issue: 1
  year: 2010
  ident: 1658_CR58
  publication-title: Cold Spring Harb Perspect Biol
  doi: 10.1101/cshperspect.a001008
– volume: 53
  start-page: 205
  issue: 2
  year: 2021
  ident: 1658_CR56
  publication-title: Pathology
  doi: 10.1016/j.pathol.2020.07
– volume: 79
  start-page: 243
  issue: 2
  year: 2021
  ident: 1658_CR3
  publication-title: Eur Urol
  doi: 10.1016/j.eururo.2020.09.042
– volume: 6
  start-page: 231
  issue: 2
  year: 2020
  ident: 1658_CR6
  publication-title: Eur Urol Focus
  doi: 10.1016/j.euf.2019.06.004
– volume: 144
  start-page: 646
  issue: 5
  year: 2011
  ident: 1658_CR63
  publication-title: Cell
  doi: 10.1016/j.cell.2011.02.013
– volume: 400
  start-page: 9
  year: 2017
  ident: 1658_CR47
  publication-title: Cancer Lett
  doi: 10.1016/j.canlet.2017.04.025
– volume: 24
  start-page: 1086
  issue: 7
  year: 2015
  ident: 1658_CR12
  publication-title: Cancer Epidemiol Biomarkers Prev
  doi: 10.1158/1055-9965.Epi-14-1329
– volume: 12
  start-page: 29
  issue: 1
  year: 2021
  ident: 1658_CR59
  publication-title: Protein Cell
  doi: 10.1007/s13238-020-00786-8
– volume: 86
  start-page: 106709
  year: 2020
  ident: 1658_CR26
  publication-title: Int Immunopharmacol
  doi: 10.1016/j.intimp.2020.106709
– volume: 120
  start-page: 2756
  issue: 3
  year: 2019
  ident: 1658_CR30
  publication-title: J Cell Biochem
  doi: 10.1002/jcb.27646
– volume: 48
  start-page: 812
  issue: 4
  year: 2018
  ident: 1658_CR28
  publication-title: Immunity
  doi: 10.1016/j.immuni.2018.03
– volume: 44
  start-page: 685
  issue: 6
  year: 2012
  ident: 1658_CR61
  publication-title: Nat Genet
  doi: 10.1038/ng.2279
– volume: 14
  start-page: 107
  issue: 2
  year: 2017
  ident: 1658_CR42
  publication-title: Nat Rev Urol
  doi: 10.1038/nrurol.2016.199
– volume: 5
  start-page: 628
  issue: 6
  year: 2022
  ident: 1658_CR8
  publication-title: Eur Urol Oncol
  doi: 10.1016/j.euo.2022.10.003
– volume: 16
  start-page: 284
  issue: 5
  year: 2012
  ident: 1658_CR21
  publication-title: Omics
  doi: 10.1089/omi.2011.0118
– volume: 14
  start-page: 634
  issue: 9
  year: 2012
  ident: 1658_CR53
  publication-title: Clin Transl Oncol
  doi: 10.1007/s12094-012-0855-6
– volume: 25
  start-page: 30
  issue: 1
  year: 2018
  ident: 1658_CR51
  publication-title: J Biomed Sci
  doi: 10.1186/s12929-018-0430-8
– volume: 13
  start-page: 859
  issue: 5
  year: 2014
  ident: 1658_CR67
  publication-title: Cell Cycle
  doi: 10.4161/cc.27767
– volume: 64
  start-page: 2212
  issue: 6
  year: 2004
  ident: 1658_CR40
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.can-2148-2
– volume: 75a
  start-page: 279
  year: 1981
  ident: 1658_CR10
  publication-title: Prog Clin Biol Res
– volume: 19
  start-page: 393
  issue: 3
  year: 2014
  ident: 1658_CR43
  publication-title: Cell Metab
  doi: 10.1016/j.cmet.2014.01.019
– volume: 11
  start-page: 583084
  year: 2020
  ident: 1658_CR29
  publication-title: Front Immunol
  doi: 10.3389/fimmu.2020.583084
– volume: 50
  start-page: 302
  issue: 2
  year: 2019
  ident: 1658_CR32
  publication-title: Immunity
  doi: 10.1016/j.immuni.2019.01.020
– volume: 33
  start-page: 657
  issue: 2–3
  year: 2014
  ident: 1658_CR5
  publication-title: Cancer Metastasis Rev
  doi: 10.1007/s10555-013-9470-4
– volume: 72
  start-page: 7
  issue: 1
  year: 2022
  ident: 1658_CR2
  publication-title: CA Cancer J Clin
  doi: 10.3322/caac.21708
– volume: 18
  start-page: 248
  issue: 1
  year: 2017
  ident: 1658_CR23
  publication-title: Cell Rep
  doi: 10.1016/j.celrep.2016.12.019
– volume: 3
  start-page: 781
  issue: 5
  year: 2010
  ident: 1658_CR54
  publication-title: Mol Med Rep
  doi: 10.3892/mmr.2010.332
– volume: 170
  start-page: 1062
  issue: 6
  year: 2017
  ident: 1658_CR57
  publication-title: Cell
  doi: 10.1016/j.cell.2017.08.028
– volume: 37
  start-page: 183
  issue: 1
  year: 2018
  ident: 1658_CR50
  publication-title: J Exp Clin Cancer Res
  doi: 10.1186/s13046-018-0851-y
– volume: 20
  start-page: 160
  issue: 1
  year: 2021
  ident: 1658_CR48
  publication-title: Mol Cancer
  doi: 10.1186/s12943-021-01452-1
– volume: 76
  start-page: 4785
  issue: 16
  year: 2016
  ident: 1658_CR14
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.Can-16-0903
– volume: 43
  start-page: e47
  issue: 7
  year: 2015
  ident: 1658_CR18
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/gkv007
– volume: 30
  start-page: 27
  issue: 1
  year: 2016
  ident: 1658_CR41
  publication-title: Cancer Cell
  doi: 10.1016/j.ccell.2016.05.004
– volume: 30
  start-page: 143
  issue: 1
  year: 2019
  ident: 1658_CR65
  publication-title: Cell Metab
  doi: 10.1016/j.cmet.2019.04.002
– volume: 48
  start-page: W509
  issue: W1
  year: 2020
  ident: 1658_CR19
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/gkaa407
– volume: 14
  start-page: 7
  year: 2013
  ident: 1658_CR20
  publication-title: BMC Bioinform
  doi: 10.1186/1471-2105-14-7
– volume: 2
  start-page: 132
  issue: 2
  year: 2020
  ident: 1658_CR39
  publication-title: Nat Metab
  doi: 10.1038/s42255-020-0174-0
– volume: 40
  start-page: 3610
  issue: 20
  year: 2021
  ident: 1658_CR52
  publication-title: Oncogene
  doi: 10.1038/s41388-021-01786-6
– volume: 15
  start-page: 1243
  issue: 12
  year: 2014
  ident: 1658_CR64
  publication-title: EMBO Rep
  doi: 10.15252/embr.201439246
– volume: 28
  start-page: 569
  issue: 5
  year: 2015
  ident: 1658_CR38
  publication-title: Cancer Cell
  doi: 10.1016/j.ccell.2015.09.021
– volume: 8
  start-page: 3438
  issue: 11
  year: 2002
  ident: 1658_CR45
  publication-title: Clin Cancer Res
– volume: 28
  start-page: 882
  issue: 6
  year: 2012
  ident: 1658_CR17
  publication-title: Bioinformatics
  doi: 10.1093/bioinformatics/bts034
– volume: 16
  start-page: 643
  year: 2016
  ident: 1658_CR13
  publication-title: BMC Cancer
  doi: 10.1186/s12885
– volume: 146
  start-page: S38
  issue: Suppl
  year: 2017
  ident: 1658_CR36
  publication-title: Indian J Med Res
  doi: 10.4103/ijmr
– volume: 52
  start-page: 790
  issue: 8
  year: 2020
  ident: 1658_CR60
  publication-title: Nat Genet
  doi: 10.1038/s41588-020-0664-8
– volume: 347
  start-page: 1260419
  issue: 6220
  year: 2015
  ident: 1658_CR24
  publication-title: Science
  doi: 10.1126/science.1260419
– volume: 18
  start-page: 1233
  issue: 11
  year: 2016
  ident: 1658_CR66
  publication-title: Nat Cell Biol
  doi: 10.1038/ncb3427
– volume: 7
  start-page: 9
  issue: 1
  year: 2021
  ident: 1658_CR33
  publication-title: Nat Rev Dis Primers
  doi: 10.1038/s41572-020-00243-0
– volume: 25
  start-page: 402
  issue: 4
  year: 2001
  ident: 1658_CR16
  publication-title: Calif)
  doi: 10.1006/meth.2001.1262
– year: 2021
  ident: 1658_CR37
  publication-title: Cancers 
  doi: 10.3390/cancers13184696
– volume: 144
  start-page: 2074
  issue: 9
  year: 2019
  ident: 1658_CR49
  publication-title: Int J Cancer
  doi: 10.1002/ijc.31817
– volume: 12
  start-page: 887854
  year: 2022
  ident: 1658_CR7
  publication-title: Front Oncol
  doi: 10.3389/fonc.2022.887854
– volume: 121
  start-page: 1461
  issue: 4
  year: 1987
  ident: 1658_CR44
  publication-title: Endocrinology
  doi: 10.1210/endo-121-4-1461
– volume: 24
  start-page: 34
  issue: 1
  year: 2018
  ident: 1658_CR46
  publication-title: Mol Med
  doi: 10.1186/s10020-018-0035-4
– volume: 140
  start-page: 16
  year: 2017
  ident: 1658_CR31
  publication-title: Biomaterials
  doi: 10.1016/j.biomaterials.2017.06.013
– volume: 79
  start-page: 44
  issue: Suppl 1
  year: 1997
  ident: 1658_CR4
  publication-title: Br J Urol
  doi: 10.1111/j.1464-410x.1997.tb00800.x
– volume: 71
  start-page: 209
  issue: 3
  year: 2021
  ident: 1658_CR1
  publication-title: CA Cancer J Clin
  doi: 10.3322/caac.21660
– volume: 21
  start-page: 252
  issue: 2
  year: 2018
  ident: 1658_CR35
  publication-title: Prostate Cancer Prostatic Dis
  doi: 10.1038/s41391-017-0030-9
– year: 2022
  ident: 1658_CR11
  publication-title: Cancers
  doi: 10.3390/cancers14174293
– year: 2020
  ident: 1658_CR9
  publication-title: Cells
  doi: 10.3390/cells9122653
– volume: 30
  start-page: 44
  issue: 1
  year: 2019
  ident: 1658_CR25
  publication-title: Ann Oncol
  doi: 10.1093/annonc/mdy495
SSID ssj0002513305
Score 2.2774844
Snippet Background Cholesterol metabolism is essential for the development and progression of prostate cancer (PCa). Our previous study provided a new insight of...
Cholesterol metabolism is essential for the development and progression of prostate cancer (PCa). Our previous study provided a new insight of cholesterol...
BackgroundCholesterol metabolism is essential for the development and progression of prostate cancer (PCa). Our previous study provided a new insight of...
Abstract Background Cholesterol metabolism is essential for the development and progression of prostate cancer (PCa). Our previous study provided a new insight...
SourceID doaj
pubmedcentral
proquest
pubmed
crossref
springer
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage 777
SubjectTerms Androgens
Cancer Research
Cancer therapies
Cell growth
Chemotherapy
Cholesterol
Cholesterol metabolism
Genes
Immunotherapy
Internal Medicine
Medical prognosis
Medicine
Medicine & Public Health
Metabolism
Molecular Medicine
Mortality
Oncology
Penicillin
Prostate cancer
Proteins
Radiation therapy
Radiotherapy
Statins
Surgical Oncology
Tumor microenvironment
Tumor mutation burden
SummonAdditionalLinks – databaseName: DOAJ Directory of Open Access Journals
  dbid: DOA
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1La9wwEBYlh9BL6btO06BCb62oJMuydUxCQiikpwZyE7IedCGxQ9YL-RX9zZ2RvJtsH_TSqyXBoPk0M0bzfSLkg6p9b3ivWKdqzlQKjjnDOfOhbVsUg9YR2cjnX_XZhfpy2Vw-eOoLe8KKPHDZuM8pCBUUFMnCaRVkb4JyRiPses19Chh9Iec9-JnCGCzx2RLezCyZwpWTupUMUhJDBk_H7rYyURbs_1OV-Xuz5C83pjkRnT4lT-YKkh4Wy5-RR3F4TnbP5zvyF-THWmeEjolOmIpyYED2McV-UIqiTQA6CqUfzUxf7IHCyRgJs3DCeEWv4wTwuFosr-lioDfIDYGqlHoEyS2FVbTwK3Fd5sPEQLEXJOuE0nGgyxUEIYDxS3JxevLt-IzNry4wr4ycmE6qM14EKWLTe62Egc03KqWgjfL489okLBSjD95xH3QbJW8DCp2FJJypX5GdYRziG0Jb5XTnAQUelvI6uMC19LFxCUJFME1FPq49YG-KuIa9l1FGf1nwl83-sncVOUInbWaiMHb-AHCxM1zsv-BSkf21i-18Wpe2Fiiy30IxV5H3m2E4Z3h54oY4rsocvOrWqiKvCyI2ltRGQ5XZiIp0W1jZMnV7ZFh8z1reRf2I1xX5tIbVvV1_34u9_7EXb8ljiedBSCa6fbIz3a7iOyixpv4gn6afoKUlaw
  priority: 102
  providerName: Directory of Open Access Journals
– databaseName: Health & Medical Collection
  dbid: 7X7
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfV1bi9QwFD7oCuKLeN_qKhF802CSpknzJCoui7A-uTBvJc1FB3bbcaYD-yv8zeak7Qzj7bVNIO35cnKSc74vAK9k6VrDWklrWTIqo7fUGsao81prFINWAdnI51_U2YX8vKgW04HbZiqrnH1idtS-d3hG_rbkKISeNt363eoHxVujMLs6XaFxE26hdBmiWi_07oxF4OUlrJq4MiNjTigtaFqYKPJ4anp9sB5l2f6_xZp_lkz-ljfNy9HpPbg7xZHk_Wj4-3AjdA_g9vmUKX8IP2e1EdJHMuCClN0DcpAJVoUSlG5K0CMpACSZ74uVUNgY_WGWT-gvyVUYEkgul5srsuzIChkiKTYlDqGyJqkXGVmW2C-zYoInWBGS1UJJ35HNNrmiBOZHcHH66evHMzrdvUCdNGKgKsraOO4FD1XrlOQm7VOMjNErIx1uYauI4WJw3lnmvNJBMO1R7sxHbk35GI66vgvHQLS0qnYJCy51ZaW3ninhQmVjchjeVAW8ni3QrEaJjWYvpoz2apK9mmyv5rqAD2ikXUuUx84P-vW3ZpptTfRcprGImlslvWiNl9Yo9FWtYi76Ak5mEzfTnN00e4QV8HL3Os02TKHYLvTbsQ0mvJUs4MmIiN1ISqNSrFnxAuoDrBwM9fBNt_yeFb1HDSRWFvBmhtV-XP_-F0___xnP4I5ApHNBeX0CR8N6G56nEGpoX-R58gumuBzb
  priority: 102
  providerName: ProQuest
Title Analysis of transcriptomic data reveals the landscape of cholesterol metabolism in prostate cancer and impact of related signature on survival
URI https://link.springer.com/article/10.1007/s12672-024-01658-x
https://www.ncbi.nlm.nih.gov/pubmed/39692951
https://www.proquest.com/docview/3146647617
https://www.proquest.com/docview/3146953664
https://pubmed.ncbi.nlm.nih.gov/PMC11656003
https://doaj.org/article/fd14d44281a64d2b9d4a964880b60cfd
Volume 15
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV1Na9wwEBVtAqWX0u-4TRcVemtFJVmWrGOzJIRCQikN7M3I-qALiR2yXuiv6G_ujOzdsGl66NWWQHieRs8avSdCPqjSt5a3itWq5Eyl4JiznDMfjDFoBq0jqpHPzvXphfq6qBaTTQ5qYe7U7z-vhNRGMlhJGApvagZ8cb8SpcFrGuZ6vt1PkXhRCa8mXcz9XXfWnmzRfx-v_Pt45J0aaV56Tp6SJxNnpF_GID8jD2L3nDw6m6riL8jvjbMI7RMdcPHJqQD1xhRPgFK0aQKYUSB7NGt78dQTNsbcl60S-kt6FQcAxOVydUWXHb1GNQjwUOoRFjcUetFRUYn9sgImBoqnP7IzKO07ulpD2gHgviQXJ8c_5qdsumeBeWXlwHRStfUiSBGr1mslLPyTWJVS0FZ5_F2tElLD6IN33AdtouQmoLVZSMLZ8hXZ6_ouHhBqlNO1h7h76MrL4ALX0sfKJUgOwVYF-biJQHM92mk0t8bJGK8G4tXkeDW_CnKEQdq2RCvs_AAQ0kwzq0lBKBiLrIXTKsjWBuWsxrzUau5TKMjhJsTNND9XTSnQVt8AfSvI--1rmFlYLnFd7NdjGyxua1WQ1yMitiMprQZeWYmC1DtY2Rnq7ptu-TO7d49-R7wsyKcNrG7H9e9v8eb_mr8ljyUiX0gm6kOyN9ys4zugT0M7Iw_NwszI_tHx-bfvszyLZnkrYpb3uv4AHZgarA
linkProvider Springer Nature
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9QwEB5VRQIuiDcpBYwEJ7BwHMdJDgjxqra021Mr7S0ktgMrtcl2NyvKn-Cn8BuZcZJdLa9brxtbcna-eWVmPgM8U5EpM1EqnqpIcFXZgheZENzYJEmIDFo7mkYeH-nRifo0iSdb8HOYhaG2ysEmekNtG0PfyF9FIRGhY9KdvJmdc7o1iqqrwxUaHSwO3PdvmLItXu9_QPk-l3Lv4_H7Ee9vFeBGZbLlulJpZkIrQxeXRivM4jHpUFVldaYMJWdxRYGQM9YUwlidOCkSS0RetgoLIl9Ck38FHa-gZC-ZJKtvOpIuSxFxP5vTTehJnUiOjpDT3FDKLzb8n78m4G-x7Z8tmr_Vab3727sJN_q4lb3tgHYLtlx9G66O-8r8HfgxsJuwpmItOUBvjmjmmVEXKiOqKIQ6w4CT-fli6ryixWR_PV1Dc8rOXIugPJ0uzti0ZjOaSMFYmBmC5pzhLtZNddI-P4XjLKMOFM9OypqaLZZo-lB57sLJpUjlHmzXTe0eAEtUoVOD2DO4VUS2sEJL4-KiQgNlsziAF4ME8llH6ZGvyZtJXjnKK_fyyi8CeEdCWq0kOm7_QzP_kvfanVc2VHgWmYaFVlaWmVVFpsk2llqYygawO4g4723EIl8jOoCnq8eo3VSyKWrXLLs1VGDXKoD7HSJWJ4kyjbFtHAaQbmBl46ibT-rpV88g3nEuiSiAlwOs1uf693-x8__XeALXRsfjw_xw_-jgIVyXhPpQ8jDdhe12vnSPMHxry8deZxh8vmwl_QXZ-1kc
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtV1Lb9QwEB5VW6nigngTKGAkOIFVx3Gc5IAQpV21lK4qRKXeQmI7sFKbLPsQ5U_wg_h1zDjJrpbXrdeNLTk734xnMjPfADxTkSkzUSqeqkhwVdmCF5kQ3NgkSYgMWjvqRj4e6YNT9e4sPtuAn30vDJVV9jbRG2rbGPpGvhOFRISOQXeyU3VlESd7w9eTr5wmSFGmtR-n0ULkyH3_huHb7NXhHsr6uZTD_Y9vD3g3YYAblck515VKMxNaGbq4NFphRI8BiKoqqzNlKFCLK3KKnLGmEMbqxEmRWCL1slVYEBETmv_NhKKiAWzu7o9OPiy_8EganSLirlOn7deTOpEcr0VOXUQpv1y7Df3QgL95un8WbP6WtfWX4fAGXO-8WPamhd1N2HD1Ldg67vL0t-FHz3XCmorN6Tr0xok6oBnVpDIijkLgM3Q_me82pjosWkzW2JM3NOfsws0Roufj2QUb12xC_SnoGTNDQJ0y3MXaHk_a53tynGVUj-K5SllTs9kCDSGq0h04vRK53IVB3dTuPrBEFTo1iESDW0VkCyu0NC4uKjRXNosDeNFLIJ-0BB_5isqZ5JWjvHIvr_wygF0S0nIlkXP7H5rp57zT9byyocKzyDQstLKyzKwqMk2WstTCVDaA7V7EeWcxZvkK3wE8XT5GXacETlG7ZtGuoXS7VgHcaxGxPEmUafR04zCAdA0ra0ddf1KPv3g-8ZaBSUQBvOxhtTrXv_-LB_9_jSewhQqavz8cHT2Ea5JAH0oeptswmE8X7hH6cvPycac0DD5dtZ7-ArwgXrc
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Analysis+of+transcriptomic+data+reveals+the+landscape+of+cholesterol+metabolism+in+prostate+cancer+and+impact+of+related+signature+on+survival&rft.jtitle=Discover.+Oncology&rft.au=Sun%2C+Jian-Xuan&rft.au=An%2C+Ye&rft.au=Xu%2C+Meng-Yao&rft.au=Ma%2C+Si-Yang&rft.date=2024-12-18&rft.issn=2730-6011&rft.eissn=2730-6011&rft.volume=15&rft.issue=1&rft.spage=777&rft_id=info:doi/10.1007%2Fs12672-024-01658-x&rft.externalDBID=NO_FULL_TEXT
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2730-6011&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2730-6011&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2730-6011&client=summon