PTOV1 promotes cisplatin-induced chemotherapy resistance by activating the nuclear factor kappa B pathway in ovarian cancer
Chemotherapy resistance is a bottleneck for ovarian cancer treatment; therefore, revealing its regulatory mechanism is critical. In the present study, we found that prostate tumor overexpressed-1 (PTOV1) was upregulated significantly in ovarian cancer cells and tissues. Patients with high PTOV1 leve...
Saved in:
| Published in | Molecular therapy. Oncolytics Vol. 20; pp. 499 - 507 |
|---|---|
| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
26.03.2021
American Society of Gene & Cell Therapy Elsevier |
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | Chemotherapy resistance is a bottleneck for ovarian cancer treatment; therefore, revealing its regulatory mechanism is critical. In the present study, we found that prostate tumor overexpressed-1 (PTOV1) was upregulated significantly in ovarian cancer cells and tissues. Patients with high PTOV1 levels had a poor outcome. In addition, PTOV1 overexpression increased CDDP (cisplatin) resistance, while PTOV1 knockdown inhibited CDDP resistance, as determined using cell viability assays, apoptosis assays, and an animal model. Mechanistic analysis showed that PTOV1 increased nuclear factor kappa B (NF-κB) pathway activity, reflected by increased nuclear translocation of its p65 subunit and the phosphorylation of inhibitor of nuclear factor kappa-B kinase subunits alpha and beta, which are markers of NF-κB pathway activation. Inhibition of the NF-κB pathway in PTOV1-overexpressing ovarian cancer cells increased CDDP-induced apoptosis, suggesting that PTOV1 promoted chemotherapy resistance by activating the NF-κB pathway. In summary, we identified PTOV1 as a prognostic factor for patients with ovarian cancer. PTOV1 might be a target for inhibition of chemotherapy resistance.
[Display omitted]
Chemotherapy resistance is a bottleneck of ovarian cancer treatment. In this study, we found PTOV1 not only served as a prognostic factor for ovarian cancer patients but also was a novel target for inhibition of cisplatin resistance. |
|---|---|
| AbstractList | Chemotherapy resistance is a bottleneck for ovarian cancer treatment; therefore, revealing its regulatory mechanism is critical. In the present study, we found that prostate tumor overexpressed-1 (PTOV1) was upregulated significantly in ovarian cancer cells and tissues. Patients with high PTOV1 levels had a poor outcome. In addition,
PTOV1
overexpression increased CDDP (cisplatin) resistance, while
PTOV1
knockdown inhibited CDDP resistance, as determined using cell viability assays, apoptosis assays, and an animal model. Mechanistic analysis showed that PTOV1 increased nuclear factor kappa B (NF-κB) pathway activity, reflected by increased nuclear translocation of its p65 subunit and the phosphorylation of inhibitor of nuclear factor kappa-B kinase subunits alpha and beta, which are markers of NF-κB pathway activation. Inhibition of the NF-κB pathway in
PTOV1
-overexpressing ovarian cancer cells increased CDDP-induced apoptosis, suggesting that PTOV1 promoted chemotherapy resistance by activating the NF-κB pathway. In summary, we identified PTOV1 as a prognostic factor for patients with ovarian cancer. PTOV1 might be a target for inhibition of chemotherapy resistance.
Chemotherapy resistance is a bottleneck of ovarian cancer treatment. In this study, we found PTOV1 not only served as a prognostic factor for ovarian cancer patients but also was a novel target for inhibition of cisplatin resistance. Chemotherapy resistance is a bottleneck for ovarian cancer treatment; therefore, revealing its regulatory mechanism is critical. In the present study, we found that prostate tumor overexpressed-1 (PTOV1) was upregulated significantly in ovarian cancer cells and tissues. Patients with high PTOV1 levels had a poor outcome. In addition, PTOV1 overexpression increased CDDP (cisplatin) resistance, while PTOV1 knockdown inhibited CDDP resistance, as determined using cell viability assays, apoptosis assays, and an animal model. Mechanistic analysis showed that PTOV1 increased nuclear factor kappa B (NF-κB) pathway activity, reflected by increased nuclear translocation of its p65 subunit and the phosphorylation of inhibitor of nuclear factor kappa-B kinase subunits alpha and beta, which are markers of NF-κB pathway activation. Inhibition of the NF-κB pathway in PTOV1-overexpressing ovarian cancer cells increased CDDP-induced apoptosis, suggesting that PTOV1 promoted chemotherapy resistance by activating the NF-κB pathway. In summary, we identified PTOV1 as a prognostic factor for patients with ovarian cancer. PTOV1 might be a target for inhibition of chemotherapy resistance. Chemotherapy resistance is a bottleneck for ovarian cancer treatment; therefore, revealing its regulatory mechanism is critical. In the present study, we found that prostate tumor overexpressed-1 (PTOV1) was upregulated significantly in ovarian cancer cells and tissues. Patients with high PTOV1 levels had a poor outcome. In addition, PTOV1 overexpression increased CDDP (cisplatin) resistance, while PTOV1 knockdown inhibited CDDP resistance, as determined using cell viability assays, apoptosis assays, and an animal model. Mechanistic analysis showed that PTOV1 increased nuclear factor kappa B (NF-κB) pathway activity, reflected by increased nuclear translocation of its p65 subunit and the phosphorylation of inhibitor of nuclear factor kappa-B kinase subunits alpha and beta, which are markers of NF-κB pathway activation. Inhibition of the NF-κB pathway in PTOV1-overexpressing ovarian cancer cells increased CDDP-induced apoptosis, suggesting that PTOV1 promoted chemotherapy resistance by activating the NF-κB pathway. In summary, we identified PTOV1 as a prognostic factor for patients with ovarian cancer. PTOV1 might be a target for inhibition of chemotherapy resistance. [Display omitted] Chemotherapy resistance is a bottleneck of ovarian cancer treatment. In this study, we found PTOV1 not only served as a prognostic factor for ovarian cancer patients but also was a novel target for inhibition of cisplatin resistance. Chemotherapy resistance is a bottleneck for ovarian cancer treatment; therefore, revealing its regulatory mechanism is critical. In the present study, we found that prostate tumor overexpressed-1 (PTOV1) was upregulated significantly in ovarian cancer cells and tissues. Patients with high PTOV1 levels had a poor outcome. In addition, PTOV1 overexpression increased CDDP (cisplatin) resistance, while PTOV1 knockdown inhibited CDDP resistance, as determined using cell viability assays, apoptosis assays, and an animal model. Mechanistic analysis showed that PTOV1 increased nuclear factor kappa B (NF-κB) pathway activity, reflected by increased nuclear translocation of its p65 subunit and the phosphorylation of inhibitor of nuclear factor kappa-B kinase subunits alpha and beta, which are markers of NF-κB pathway activation. Inhibition of the NF-κB pathway in PTOV1-overexpressing ovarian cancer cells increased CDDP-induced apoptosis, suggesting that PTOV1 promoted chemotherapy resistance by activating the NF-κB pathway. In summary, we identified PTOV1 as a prognostic factor for patients with ovarian cancer. PTOV1 might be a target for inhibition of chemotherapy resistance.Chemotherapy resistance is a bottleneck for ovarian cancer treatment; therefore, revealing its regulatory mechanism is critical. In the present study, we found that prostate tumor overexpressed-1 (PTOV1) was upregulated significantly in ovarian cancer cells and tissues. Patients with high PTOV1 levels had a poor outcome. In addition, PTOV1 overexpression increased CDDP (cisplatin) resistance, while PTOV1 knockdown inhibited CDDP resistance, as determined using cell viability assays, apoptosis assays, and an animal model. Mechanistic analysis showed that PTOV1 increased nuclear factor kappa B (NF-κB) pathway activity, reflected by increased nuclear translocation of its p65 subunit and the phosphorylation of inhibitor of nuclear factor kappa-B kinase subunits alpha and beta, which are markers of NF-κB pathway activation. Inhibition of the NF-κB pathway in PTOV1-overexpressing ovarian cancer cells increased CDDP-induced apoptosis, suggesting that PTOV1 promoted chemotherapy resistance by activating the NF-κB pathway. In summary, we identified PTOV1 as a prognostic factor for patients with ovarian cancer. PTOV1 might be a target for inhibition of chemotherapy resistance. Chemotherapy resistance is a bottleneck for ovarian cancer treatment; therefore, revealing its regulatory mechanism is critical. In the present study, we found that prostate tumor overexpressed-1 (PTOV1) was upregulated significantly in ovarian cancer cells and tissues. Patients with high PTOV1 levels had a poor outcome. In addition, overexpression increased CDDP (cisplatin) resistance, while knockdown inhibited CDDP resistance, as determined using cell viability assays, apoptosis assays, and an animal model. Mechanistic analysis showed that PTOV1 increased nuclear factor kappa B (NF-κB) pathway activity, reflected by increased nuclear translocation of its p65 subunit and the phosphorylation of inhibitor of nuclear factor kappa-B kinase subunits alpha and beta, which are markers of NF-κB pathway activation. Inhibition of the NF-κB pathway in -overexpressing ovarian cancer cells increased CDDP-induced apoptosis, suggesting that PTOV1 promoted chemotherapy resistance by activating the NF-κB pathway. In summary, we identified PTOV1 as a prognostic factor for patients with ovarian cancer. PTOV1 might be a target for inhibition of chemotherapy resistance. |
| Author | He, Shanyang Liao, Bing Lan, Jin Wan, Zhiyong You, Zeshan Shen, Hongwei Zhao, Yunhe Liu, Jun |
| Author_xml | – sequence: 1 givenname: Hongwei surname: Shen fullname: Shen, Hongwei organization: Department of Obstetrics and Gynecology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, Guangdong, China – sequence: 2 givenname: Bing surname: Liao fullname: Liao, Bing organization: Department of Obstetrics and Gynecology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, Guangdong, China – sequence: 3 givenname: Zhiyong surname: Wan fullname: Wan, Zhiyong organization: Department of Obstetrics and Gynecology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, Guangdong, China – sequence: 4 givenname: Yunhe surname: Zhao fullname: Zhao, Yunhe organization: Department of Obstetrics and Gynecology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, Guangdong, China – sequence: 5 givenname: Zeshan surname: You fullname: You, Zeshan organization: Department of Obstetrics and Gynecology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, Guangdong, China – sequence: 6 givenname: Jun surname: Liu fullname: Liu, Jun organization: Department of Obstetrics and Gynecology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, Guangdong, China – sequence: 7 givenname: Jin surname: Lan fullname: Lan, Jin organization: Department of Obstetrics and Gynecology, the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, Guangdong, China – sequence: 8 givenname: Shanyang surname: He fullname: He, Shanyang email: drhsy8899@126.com organization: Department of Obstetrics and Gynecology, Guangdong Provincial People’s Hospital and Guangdong Academy of Medical Sciences, Guangzhou 510080, Guangdong Province, China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33738336$$D View this record in MEDLINE/PubMed |
| BookMark | eNp9kl9vFCEUxSemxtbaL-CD4dGXXfkzDExiTLSx2qRJfai-EgYuu6yzMAK7ZuOXL-u2pvWhTxDuOb8LnPuyOQoxQNO8JnhOMOnereZxXeKcYkrmmM4xls-aE8oEnQmB-dGD_XFzlvMKY0zaTvacvWiOGRNMMtadNH--3Vz_IGhKcR0LZGR8nkZdfJj5YDcGLDJLqKUlJD3tUILsc9HBABp2SJvit3vxAlUBChszgk7I1fOY0E89TRp9QpMuy996h3xAcauT1wGZPSG9ap47PWY4u1tPm-8Xn2_Ov86urr9cnn-8mhlOSZnxHgSVgnQ9wCCFs05LLhjgnkreOmONkMIK65jrNQPTgnZyIBJDx4AIxk6bywPXRr1SU_JrnXYqaq_-HsS0UDoVXy-vqCBmsAQ6jkWrjeuH3gjmWm6cc21vK-vDgTVthjVYA6EkPT6CPq4Ev1SLuFWiZ4J3pALe3gFS_LWBXNTaZwPjqAPETVaUY9ayriW8St887PWvyX16VSAPApNizgmcMr7UPOK-tR8VwWo_K6q-sc6K2s-KwlTVWalW-p_1nv6k6f3BBDWtrYeksvFQo7Q-gSn1O_1T9luB2Nuz |
| CitedBy_id | crossref_primary_10_18311_jnr_2023_32092 crossref_primary_10_1089_aivt_2023_0010 crossref_primary_10_1038_s42003_025_07930_2 crossref_primary_10_2174_1568009623666230316153813 crossref_primary_10_1186_s12943_024_01967_3 crossref_primary_10_62347_OCKH4789 crossref_primary_10_2139_ssrn_3916764 crossref_primary_10_1007_s11418_024_01783_5 crossref_primary_10_1111_jcmm_17004 crossref_primary_10_18632_aging_204211 |
| Cites_doi | 10.1007/s00280-013-2241-7 10.1517/13543784.2015.1062874 10.1007/s00428-010-1018-1 10.1186/1471-2407-14-457 10.1038/onc.2011.384 10.7150/jca.29889 10.1006/meth.2001.1262 10.1371/journal.pone.0136448 10.1016/j.biocel.2018.03.015 10.1038/sj.onc.1204233 10.1016/j.cmet.2010.12.008 10.1186/1476-4598-13-74 10.1007/s13277-014-2662-x 10.1038/nrc1588 10.1158/1078-0432.CCR-07-4987 10.1007/s12013-014-0179-y 10.1182/blood-2017-06-792150 10.1016/j.trsl.2013.10.002 10.1038/onc.2013.51 10.1097/PAS.0b013e318212ae22 10.1016/j.omtn.2019.05.007 10.1038/embor.2009.243 10.1016/S0002-9440(10)63885-0 10.1186/1476-4598-10-10 10.1007/s00432-015-2107-y 10.1126/stke.3572006re13 10.1002/jcp.26125 10.18632/oncotarget.8103 10.1177/1010428317705013 |
| ContentType | Journal Article |
| Copyright | 2021 2021. 2021. 2021 |
| Copyright_xml | – notice: 2021 – notice: 2021. – notice: 2021. 2021 |
| DBID | 6I. AAFTH AAYXX CITATION NPM 7X8 5PM DOA |
| DOI | 10.1016/j.omto.2021.02.008 |
| DatabaseName | ScienceDirect Open Access Titles Elsevier:ScienceDirect:Open Access CrossRef PubMed MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals |
| DatabaseTitle | CrossRef PubMed MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic PubMed |
| Database_xml | – sequence: 1 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 2 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 |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine |
| EISSN | 2372-7705 |
| EndPage | 507 |
| ExternalDocumentID | oai_doaj_org_article_271cbd1e65074acf9b9c73f45cfff49d PMC7937561 33738336 10_1016_j_omto_2021_02_008 S2372770521000267 |
| Genre | Journal Article |
| GroupedDBID | 0R~ 0SF 53G 5VS 6I. 7X7 8FE 8FH 8FI AACTN AAEDW AAFTH AALRI AAXUO ABMAC ACGFS ADBBV AFKRA AFTJW AITUG ALMA_UNASSIGNED_HOLDINGS AMRAJ AOIJS BBNVY BCNDV BENPR BHPHI BPHCQ BVXVI EBS FDB FYUFA GROUPED_DOAJ HCIFZ HYE HZ~ LK8 M41 M48 M7P M~E NCXOZ O9- OK1 PIMPY PQQKQ PROAC ROL RPM SSZ 8FJ AAYWO AAYXX ABUWG ADRAZ ADVLN ALIPV CCPQU CITATION EJD HMCUK PHGZM PHGZT UKHRP NPM 7X8 5PM |
| ID | FETCH-LOGICAL-c521t-59e7287169eeb87fdfa8573e092854fcdc787d7df3f9a3ec4eaf8b180e63e1733 |
| IEDL.DBID | M48 |
| ISSN | 2372-7705 |
| IngestDate | Wed Aug 27 01:08:09 EDT 2025 Thu Aug 21 18:17:36 EDT 2025 Fri Jul 11 14:53:39 EDT 2025 Thu Jan 02 22:56:57 EST 2025 Thu Apr 24 23:03:52 EDT 2025 Tue Jul 01 00:47:21 EDT 2025 Tue May 16 22:23:38 EDT 2023 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Keywords | PTOV1 chemotherapy resistance ovarian cancer NF-κB pathway |
| Language | English |
| License | This is an open access article under the CC BY-NC-ND license. 2021. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c521t-59e7287169eeb87fdfa8573e092854fcdc787d7df3f9a3ec4eaf8b180e63e1733 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally |
| OpenAccessLink | http://journals.scholarsportal.info/openUrl.xqy?doi=10.1016/j.omto.2021.02.008 |
| PMID | 33738336 |
| PQID | 2503436415 |
| PQPubID | 23479 |
| PageCount | 9 |
| ParticipantIDs | doaj_primary_oai_doaj_org_article_271cbd1e65074acf9b9c73f45cfff49d pubmedcentral_primary_oai_pubmedcentral_nih_gov_7937561 proquest_miscellaneous_2503436415 pubmed_primary_33738336 crossref_citationtrail_10_1016_j_omto_2021_02_008 crossref_primary_10_1016_j_omto_2021_02_008 elsevier_sciencedirect_doi_10_1016_j_omto_2021_02_008 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2021-03-26 |
| PublicationDateYYYYMMDD | 2021-03-26 |
| PublicationDate_xml | – month: 03 year: 2021 text: 2021-03-26 day: 26 |
| PublicationDecade | 2020 |
| PublicationPlace | United States |
| PublicationPlace_xml | – name: United States |
| PublicationTitle | Molecular therapy. Oncolytics |
| PublicationTitleAlternate | Mol Ther Oncolytics |
| PublicationYear | 2021 |
| Publisher | Elsevier Inc American Society of Gene & Cell Therapy Elsevier |
| Publisher_xml | – name: Elsevier Inc – name: American Society of Gene & Cell Therapy – name: Elsevier |
| References | Galluzzi, Senovilla, Vitale, Michels, Martins, Kepp, Castedo, Kroemer (bib21) 2012; 31 Baker, Hayden, Ghosh (bib25) 2011; 13 Song, Kim, Lee, Choi, Kim, Lee, Kim, Bae (bib3) 2013; 72 Rausch, Hennenlotter, Scharpf, Teepe, Kühs, Aufderklamm, Bier, Mischinger, Gakis, Stenzl (bib11) 2016; 142 Bollrath, Greten (bib26) 2009; 10 Häcker, Karin (bib27) 2006; 2006 Marqués, Sesé, Cánovas, Valente, Bermudo, de Torres, Fernández, Abasolo, Fernández, Contreras (bib8) 2014; 33 Fernández, Mosquera, Alaña, Sanchez-Pla, Morote, Ramón Y Cajal, Reventós, de Torres, Paciucci (bib13) 2011; 458 Wang, Li, Zhou, Li, Cai, Shi, Liu (bib4) 2019; 10 Santamaría, Fernández, Farré, Benedit, Reventós, Morote, Paciucci, Thomson (bib6) 2003; 162 Li, Leng, Liu, Hu, Zhang, Li, Jiang, Zhou, Xu (bib10) 2017; 39 Alaña, Sesé, Cánovas, Punyal, Fernández, Abasolo, de Torres, Ruiz, Espinosa, Bigas (bib7) 2014; 13 Chian, Chiang, Chuang, Liu (bib18) 2014; 163 Morote, Fernández, Alaña, Iglesias, Planas, Reventós, Ramón Y Cajal, Paciucci, de Torres (bib9) 2008; 14 Sun, Huang, Chang, Chao (bib23) 2018; 233 Lei, Zhang, Li, Lin, Wu, Li, Liu (bib15) 2014; 14 Guo, Feng, Zhang, Xu, Li, Kung, Song, Zeng (bib29) 2011; 10 Nakanishi, Toi (bib24) 2005; 5 Momeny, Yousefi, Eyvani, Moghaddaskho, Salehi, Esmaeili, Alishahi, Barghi, Vaezijoze, Shamsaiegahkani (bib22) 2018; 99 Yang, Lin, Wu, Lei, Zhu, Song, Hong, Guo (bib12) 2015; 10 Guo, Feng, Hu, Wang, Luo, Zhong, Deng (bib16) 2015; 36 Livak, Schmittgen (bib28) 2001; 25 Cyrenne, Lewis, Weed, Carlson, Mirza, Foss, Girardi (bib19) 2017; 130 Yang, Wang, Wang, He, Chen, Liang, He, Wu, Song, Chen (bib14) 2016; 7 Bogliolo, Cassani, Gardella, Musacchi, Babilonti, Venturini, Ferrero, Spinillo (bib2) 2015; 24 Benedit, Paciucci, Thomson, Valeri, Nadal, Càceres, de Torres, Estivill, Lozano, Morote, Reventós (bib5) 2001; 20 Li, Niu, Qin, Yang, Wang, Yu, Wei, Jin, Wang, Yang, Chen (bib1) 2019; 17 King, Tung, Tsang, Zu, Lok, Deavers, Malpica, Wolf, Lu, Birrer (bib17) 2011; 35 Yin, Wang, Zhang, Jiang, Lu, Wei, Huo, Xiao, Ou (bib20) 2015; 71 King (10.1016/j.omto.2021.02.008_bib17) 2011; 35 Häcker (10.1016/j.omto.2021.02.008_bib27) 2006; 2006 Rausch (10.1016/j.omto.2021.02.008_bib11) 2016; 142 Wang (10.1016/j.omto.2021.02.008_bib4) 2019; 10 Momeny (10.1016/j.omto.2021.02.008_bib22) 2018; 99 Li (10.1016/j.omto.2021.02.008_bib10) 2017; 39 Cyrenne (10.1016/j.omto.2021.02.008_bib19) 2017; 130 Santamaría (10.1016/j.omto.2021.02.008_bib6) 2003; 162 Bogliolo (10.1016/j.omto.2021.02.008_bib2) 2015; 24 Morote (10.1016/j.omto.2021.02.008_bib9) 2008; 14 Yin (10.1016/j.omto.2021.02.008_bib20) 2015; 71 Li (10.1016/j.omto.2021.02.008_bib1) 2019; 17 Song (10.1016/j.omto.2021.02.008_bib3) 2013; 72 Chian (10.1016/j.omto.2021.02.008_bib18) 2014; 163 Alaña (10.1016/j.omto.2021.02.008_bib7) 2014; 13 Nakanishi (10.1016/j.omto.2021.02.008_bib24) 2005; 5 Fernández (10.1016/j.omto.2021.02.008_bib13) 2011; 458 Sun (10.1016/j.omto.2021.02.008_bib23) 2018; 233 Bollrath (10.1016/j.omto.2021.02.008_bib26) 2009; 10 Marqués (10.1016/j.omto.2021.02.008_bib8) 2014; 33 Yang (10.1016/j.omto.2021.02.008_bib12) 2015; 10 Baker (10.1016/j.omto.2021.02.008_bib25) 2011; 13 Livak (10.1016/j.omto.2021.02.008_bib28) 2001; 25 Galluzzi (10.1016/j.omto.2021.02.008_bib21) 2012; 31 Yang (10.1016/j.omto.2021.02.008_bib14) 2016; 7 Guo (10.1016/j.omto.2021.02.008_bib16) 2015; 36 Benedit (10.1016/j.omto.2021.02.008_bib5) 2001; 20 Lei (10.1016/j.omto.2021.02.008_bib15) 2014; 14 Guo (10.1016/j.omto.2021.02.008_bib29) 2011; 10 |
| References_xml | – volume: 36 start-page: 453 year: 2015 end-page: 458 ident: bib16 article-title: Increased PTOV1 expression is related to poor prognosis in epithelial ovarian cancer publication-title: Tumour Biol. – volume: 10 start-page: 10 year: 2011 ident: bib29 article-title: Bmi-1 promotes invasion and metastasis, and its elevated expression is correlated with an advanced stage of breast cancer publication-title: Mol. Cancer – volume: 24 start-page: 1275 year: 2015 end-page: 1286 ident: bib2 article-title: Oxaliplatin for the treatment of ovarian cancer publication-title: Expert Opin. Investig. Drugs – volume: 10 start-page: e0136448 year: 2015 ident: bib12 article-title: Prostate Tumor Overexpressed 1 (PTOV1) Is a Novel Prognostic Marker for Nasopharyngeal Carcinoma Progression and Poor Survival Outcomes publication-title: PLoS ONE – volume: 13 start-page: 11 year: 2011 end-page: 22 ident: bib25 article-title: NF-κB, inflammation, and metabolic disease publication-title: Cell Metab. – volume: 142 start-page: 937 year: 2016 end-page: 947 ident: bib11 article-title: Prostate tumor overexpressed 1 expression in invasive urothelial carcinoma publication-title: J. Cancer Res. Clin. Oncol. – volume: 458 start-page: 323 year: 2011 end-page: 330 ident: bib13 article-title: PTOV1 is overexpressed in human high-grade malignant tumors publication-title: Virchows Arch. – volume: 7 start-page: 31878 year: 2016 end-page: 31891 ident: bib14 article-title: Prostate tumor overexpressed-1, in conjunction with human papillomavirus status, predicts outcome in early-stage human laryngeal squamous cell carcinoma publication-title: Oncotarget – volume: 10 start-page: 1314 year: 2009 end-page: 1319 ident: bib26 article-title: IKK/NF-kappaB and STAT3 pathways: central signalling hubs in inflammation-mediated tumour promotion and metastasis publication-title: EMBO Rep. – volume: 2006 start-page: re13 year: 2006 ident: bib27 article-title: Regulation and function of IKK and IKK-related kinases publication-title: Sci. STKE – volume: 130 start-page: 2073 year: 2017 end-page: 2083 ident: bib19 article-title: Synergy of BCL2 and histone deacetylase inhibition against leukemic cells from cutaneous T-cell lymphoma patients publication-title: Blood – volume: 35 start-page: 904 year: 2011 end-page: 912 ident: bib17 article-title: The anterior gradient homolog 3 (AGR3) gene is associated with differentiation and survival in ovarian cancer publication-title: Am. J. Surg. Pathol. – volume: 99 start-page: 1 year: 2018 end-page: 9 ident: bib22 article-title: Blockade of nuclear factor-κB (NF-κB) pathway inhibits growth and induces apoptosis in chemoresistant ovarian carcinoma cells publication-title: Int. J. Biochem. Cell Biol. – volume: 33 start-page: 1124 year: 2014 end-page: 1134 ident: bib8 article-title: Regulation of protein translation and c-Jun expression by prostate tumor overexpressed 1 publication-title: Oncogene – volume: 31 start-page: 1869 year: 2012 end-page: 1883 ident: bib21 article-title: Molecular mechanisms of cisplatin resistance publication-title: Oncogene – volume: 39 year: 2017 ident: bib10 article-title: Overexpressed PTOV1 associates with tumorigenesis and progression of esophageal squamous cell carcinoma publication-title: Tumour Biol. – volume: 10 start-page: 1800 year: 2019 end-page: 1807 ident: bib4 article-title: CUEDC2 Contributes to Cisplatin-Based Chemotherapy Resistance in Ovarian Serious Carcinoma by Regulating p38 MAPK Signaling publication-title: J. Cancer – volume: 17 start-page: 92 year: 2019 end-page: 101 ident: bib1 article-title: lncRNA UCA1 Mediates Resistance to Cisplatin by Regulating the miR-143/FOSL2-Signaling Pathway in Ovarian Cancer publication-title: Mol. Ther. Nucleic Acids – volume: 20 start-page: 1455 year: 2001 end-page: 1464 ident: bib5 article-title: PTOV1, a novel protein overexpressed in prostate cancer containing a new class of protein homology blocks publication-title: Oncogene – volume: 14 start-page: 457 year: 2014 ident: bib15 article-title: Overexpression of prostate tumor overexpressed 1 correlates with tumor progression and predicts poor prognosis in breast cancer publication-title: BMC Cancer – volume: 71 start-page: 161 year: 2015 end-page: 165 ident: bib20 article-title: Specific siRNA inhibits XIAP expression in human endometrial carcinoma cell apoptosis publication-title: Cell Biochem. Biophys. – volume: 72 start-page: 653 year: 2013 end-page: 660 ident: bib3 article-title: Phase II study of ifosfamide and cisplatin for the treatment of recurrent ovarian cancer publication-title: Cancer Chemother. Pharmacol. – volume: 13 start-page: 74 year: 2014 ident: bib7 article-title: Prostate tumor OVerexpressed-1 (PTOV1) down-regulates HES1 and HEY1 notch targets genes and promotes prostate cancer progression publication-title: Mol. Cancer – volume: 163 start-page: 211 year: 2014 end-page: 220 ident: bib18 article-title: Inhibitor of nuclear factor-κB, SN50, attenuates lipopolysaccharide-induced lung injury in an isolated and perfused rat lung model publication-title: Transl. Res. – volume: 25 start-page: 402 year: 2001 end-page: 408 ident: bib28 article-title: Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method publication-title: Methods – volume: 14 start-page: 2617 year: 2008 end-page: 2622 ident: bib9 article-title: PTOV1 expression predicts prostate cancer in men with isolated high-grade prostatic intraepithelial neoplasia in needle biopsy publication-title: Clin. Cancer Res. – volume: 162 start-page: 897 year: 2003 end-page: 905 ident: bib6 article-title: PTOV-1, a novel protein overexpressed in prostate cancer, shuttles between the cytoplasm and the nucleus and promotes entry into the S phase of the cell division cycle publication-title: Am. J. Pathol. – volume: 233 start-page: 2489 year: 2018 end-page: 2501 ident: bib23 article-title: TLR4 and NFκB signaling is critical for taxol resistance in ovarian carcinoma cells publication-title: J. Cell. Physiol. – volume: 5 start-page: 297 year: 2005 end-page: 309 ident: bib24 article-title: Nuclear factor-kappaB inhibitors as sensitizers to anticancer drugs publication-title: Nat. Rev. Cancer – volume: 72 start-page: 653 year: 2013 ident: 10.1016/j.omto.2021.02.008_bib3 article-title: Phase II study of ifosfamide and cisplatin for the treatment of recurrent ovarian cancer publication-title: Cancer Chemother. Pharmacol. doi: 10.1007/s00280-013-2241-7 – volume: 24 start-page: 1275 year: 2015 ident: 10.1016/j.omto.2021.02.008_bib2 article-title: Oxaliplatin for the treatment of ovarian cancer publication-title: Expert Opin. Investig. Drugs doi: 10.1517/13543784.2015.1062874 – volume: 458 start-page: 323 year: 2011 ident: 10.1016/j.omto.2021.02.008_bib13 article-title: PTOV1 is overexpressed in human high-grade malignant tumors publication-title: Virchows Arch. doi: 10.1007/s00428-010-1018-1 – volume: 14 start-page: 457 year: 2014 ident: 10.1016/j.omto.2021.02.008_bib15 article-title: Overexpression of prostate tumor overexpressed 1 correlates with tumor progression and predicts poor prognosis in breast cancer publication-title: BMC Cancer doi: 10.1186/1471-2407-14-457 – volume: 31 start-page: 1869 year: 2012 ident: 10.1016/j.omto.2021.02.008_bib21 article-title: Molecular mechanisms of cisplatin resistance publication-title: Oncogene doi: 10.1038/onc.2011.384 – volume: 10 start-page: 1800 year: 2019 ident: 10.1016/j.omto.2021.02.008_bib4 article-title: CUEDC2 Contributes to Cisplatin-Based Chemotherapy Resistance in Ovarian Serious Carcinoma by Regulating p38 MAPK Signaling publication-title: J. Cancer doi: 10.7150/jca.29889 – volume: 25 start-page: 402 year: 2001 ident: 10.1016/j.omto.2021.02.008_bib28 article-title: Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method publication-title: Methods doi: 10.1006/meth.2001.1262 – volume: 10 start-page: e0136448 year: 2015 ident: 10.1016/j.omto.2021.02.008_bib12 article-title: Prostate Tumor Overexpressed 1 (PTOV1) Is a Novel Prognostic Marker for Nasopharyngeal Carcinoma Progression and Poor Survival Outcomes publication-title: PLoS ONE doi: 10.1371/journal.pone.0136448 – volume: 99 start-page: 1 year: 2018 ident: 10.1016/j.omto.2021.02.008_bib22 article-title: Blockade of nuclear factor-κB (NF-κB) pathway inhibits growth and induces apoptosis in chemoresistant ovarian carcinoma cells publication-title: Int. J. Biochem. Cell Biol. doi: 10.1016/j.biocel.2018.03.015 – volume: 20 start-page: 1455 year: 2001 ident: 10.1016/j.omto.2021.02.008_bib5 article-title: PTOV1, a novel protein overexpressed in prostate cancer containing a new class of protein homology blocks publication-title: Oncogene doi: 10.1038/sj.onc.1204233 – volume: 13 start-page: 11 year: 2011 ident: 10.1016/j.omto.2021.02.008_bib25 article-title: NF-κB, inflammation, and metabolic disease publication-title: Cell Metab. doi: 10.1016/j.cmet.2010.12.008 – volume: 13 start-page: 74 year: 2014 ident: 10.1016/j.omto.2021.02.008_bib7 article-title: Prostate tumor OVerexpressed-1 (PTOV1) down-regulates HES1 and HEY1 notch targets genes and promotes prostate cancer progression publication-title: Mol. Cancer doi: 10.1186/1476-4598-13-74 – volume: 36 start-page: 453 year: 2015 ident: 10.1016/j.omto.2021.02.008_bib16 article-title: Increased PTOV1 expression is related to poor prognosis in epithelial ovarian cancer publication-title: Tumour Biol. doi: 10.1007/s13277-014-2662-x – volume: 5 start-page: 297 year: 2005 ident: 10.1016/j.omto.2021.02.008_bib24 article-title: Nuclear factor-kappaB inhibitors as sensitizers to anticancer drugs publication-title: Nat. Rev. Cancer doi: 10.1038/nrc1588 – volume: 14 start-page: 2617 year: 2008 ident: 10.1016/j.omto.2021.02.008_bib9 article-title: PTOV1 expression predicts prostate cancer in men with isolated high-grade prostatic intraepithelial neoplasia in needle biopsy publication-title: Clin. Cancer Res. doi: 10.1158/1078-0432.CCR-07-4987 – volume: 71 start-page: 161 year: 2015 ident: 10.1016/j.omto.2021.02.008_bib20 article-title: Specific siRNA inhibits XIAP expression in human endometrial carcinoma cell apoptosis publication-title: Cell Biochem. Biophys. doi: 10.1007/s12013-014-0179-y – volume: 130 start-page: 2073 year: 2017 ident: 10.1016/j.omto.2021.02.008_bib19 article-title: Synergy of BCL2 and histone deacetylase inhibition against leukemic cells from cutaneous T-cell lymphoma patients publication-title: Blood doi: 10.1182/blood-2017-06-792150 – volume: 163 start-page: 211 year: 2014 ident: 10.1016/j.omto.2021.02.008_bib18 article-title: Inhibitor of nuclear factor-κB, SN50, attenuates lipopolysaccharide-induced lung injury in an isolated and perfused rat lung model publication-title: Transl. Res. doi: 10.1016/j.trsl.2013.10.002 – volume: 33 start-page: 1124 year: 2014 ident: 10.1016/j.omto.2021.02.008_bib8 article-title: Regulation of protein translation and c-Jun expression by prostate tumor overexpressed 1 publication-title: Oncogene doi: 10.1038/onc.2013.51 – volume: 35 start-page: 904 year: 2011 ident: 10.1016/j.omto.2021.02.008_bib17 article-title: The anterior gradient homolog 3 (AGR3) gene is associated with differentiation and survival in ovarian cancer publication-title: Am. J. Surg. Pathol. doi: 10.1097/PAS.0b013e318212ae22 – volume: 17 start-page: 92 year: 2019 ident: 10.1016/j.omto.2021.02.008_bib1 article-title: lncRNA UCA1 Mediates Resistance to Cisplatin by Regulating the miR-143/FOSL2-Signaling Pathway in Ovarian Cancer publication-title: Mol. Ther. Nucleic Acids doi: 10.1016/j.omtn.2019.05.007 – volume: 10 start-page: 1314 year: 2009 ident: 10.1016/j.omto.2021.02.008_bib26 article-title: IKK/NF-kappaB and STAT3 pathways: central signalling hubs in inflammation-mediated tumour promotion and metastasis publication-title: EMBO Rep. doi: 10.1038/embor.2009.243 – volume: 162 start-page: 897 year: 2003 ident: 10.1016/j.omto.2021.02.008_bib6 article-title: PTOV-1, a novel protein overexpressed in prostate cancer, shuttles between the cytoplasm and the nucleus and promotes entry into the S phase of the cell division cycle publication-title: Am. J. Pathol. doi: 10.1016/S0002-9440(10)63885-0 – volume: 10 start-page: 10 year: 2011 ident: 10.1016/j.omto.2021.02.008_bib29 article-title: Bmi-1 promotes invasion and metastasis, and its elevated expression is correlated with an advanced stage of breast cancer publication-title: Mol. Cancer doi: 10.1186/1476-4598-10-10 – volume: 142 start-page: 937 year: 2016 ident: 10.1016/j.omto.2021.02.008_bib11 article-title: Prostate tumor overexpressed 1 expression in invasive urothelial carcinoma publication-title: J. Cancer Res. Clin. Oncol. doi: 10.1007/s00432-015-2107-y – volume: 2006 start-page: re13 year: 2006 ident: 10.1016/j.omto.2021.02.008_bib27 article-title: Regulation and function of IKK and IKK-related kinases publication-title: Sci. STKE doi: 10.1126/stke.3572006re13 – volume: 233 start-page: 2489 year: 2018 ident: 10.1016/j.omto.2021.02.008_bib23 article-title: TLR4 and NFκB signaling is critical for taxol resistance in ovarian carcinoma cells publication-title: J. Cell. Physiol. doi: 10.1002/jcp.26125 – volume: 7 start-page: 31878 year: 2016 ident: 10.1016/j.omto.2021.02.008_bib14 article-title: Prostate tumor overexpressed-1, in conjunction with human papillomavirus status, predicts outcome in early-stage human laryngeal squamous cell carcinoma publication-title: Oncotarget doi: 10.18632/oncotarget.8103 – volume: 39 year: 2017 ident: 10.1016/j.omto.2021.02.008_bib10 article-title: Overexpressed PTOV1 associates with tumorigenesis and progression of esophageal squamous cell carcinoma publication-title: Tumour Biol. doi: 10.1177/1010428317705013 |
| SSID | ssj0001468953 |
| Score | 2.2185996 |
| Snippet | Chemotherapy resistance is a bottleneck for ovarian cancer treatment; therefore, revealing its regulatory mechanism is critical. In the present study, we found... |
| SourceID | doaj pubmedcentral proquest pubmed crossref elsevier |
| SourceType | Open Website Open Access Repository Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 499 |
| SubjectTerms | chemotherapy resistance NF-κB pathway Original ovarian cancer PTOV1 |
| SummonAdditionalLinks | – databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQDxUXxJvwqIzEDUUkceLHkaJWFRKPQ4t6s2zHhoXWG-1uQSv-PDOOd7UpUrlwTRwn9owz39gz3xDyihtnPO9sKVQAB4VhIXdb9SU3XASAsMHZFOX7kZ-cte_Pu_OdUl8YEzbSA48T96YRtbN9Df2BsTMuKKucYKHtXAihVT3-fcHm7ThTaXel5VIlCsqGCYSQVZczZsbgrvnlCjP_mkzYKSdWKZH3T4zT3-DzegzljlE6vkvuZDRJ346juEdu-Xif7H_I5-UPyO_Pp5--1HRIMXd-Sd1sOWDwWyzBFQeh9hRkdpmTsNYUXG-Ek6AH1K4ppjzghm38SqEBjch8bBZ0rNBDf5hhMPSQYknjX2ZNZ5HOf4LjbSJ12MPiITk7Pjp9d1Lmcgulw6oGZae8SP6T8t5KEfpgZCeYrxRmWQbXO1jcvegDC8ow71pvgrS1rDxnvhaMPSJ7cR79E0KNbEJwvsH_R9uABw5uiwQsxWWwxlhWkHoz3dplLnIsiXGhN0Fn3zWKSKOIdNVoEFFBXm-fGUYmjhtbH6IUty2RRTtdAN3SWbf0v3SrIN1GB3QGJCPQgK5mN7785UZhNKxWPIIx0c-vlhoAJ2sZB9RUkMejAm0_kSHJFGO8IGKiWpMxTO_E2bfECI4khwCEn_6PQT8jt3EoGGfX8Odkb7W48i8AeK3sQVpjfwD-FC54 priority: 102 providerName: Directory of Open Access Journals |
| Title | PTOV1 promotes cisplatin-induced chemotherapy resistance by activating the nuclear factor kappa B pathway in ovarian cancer |
| URI | https://dx.doi.org/10.1016/j.omto.2021.02.008 https://www.ncbi.nlm.nih.gov/pubmed/33738336 https://www.proquest.com/docview/2503436415 https://pubmed.ncbi.nlm.nih.gov/PMC7937561 https://doaj.org/article/271cbd1e65074acf9b9c73f45cfff49d |
| Volume | 20 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Nb9QwELVKkapeEN-kQGUkbihoEyd2ckCIIqoKqcChi3qzbMcuC60TstvCij_PjONsWah64Lqxs0lmJn7jzLxHyHOujLK81KmoHSQoDIXc9aRJueLCAYR1Rocq3w_8YFq8Py6PN8godxQf4PzK1A71pKb96cuf35evIeBfXdZqtWcLbOTLI_9mdYPchJVJoKLBYYT7Yc-l4FVdstg7c_XUbbLFkO2HBdLmy6UqMPqvrVj_ItK_Cyv_WKn2b5NbEWLSN4NP3CEb1t8lW4fxI_o98uvT0cfPGe1CIZ6dUzObd1gR51PIz8HSDQVDnsXOrCWFfBwxJjgH1UuKfRC4i-tPKAygHumQVU8H2R76TXWdonsUdY5_qCWdedpeQDauPDV4hv4-me6_O3p7kEYNhtSg1EFa1laEpKq2VlfCNU5VpWB2UmPrpTONgYhvROOYqxWzprDKVTqrJpYzmwnGHpBN33r7iFBV5c4Zm-NLpcghLYdcpgKAxSunldIsIdn4uKWJBOWok3Eqx0q0rxKtJdFacpJLsFZCXqzmdAM9x7Wj99CKq5FIrR1-aPsTGSNV5iIzusnAgQFdKeNqXRvBXFEa51xRNwkpRx-QEaUM6ANONbv2z5-NDiMhhPG7jPK2PZ9LQKGsYBygVEIeDg60usTRFxMi1lxr7R7Wj_jZl0ATjsyHgI53_nvmY7KN148Vdzl_QjYX_bl9ChBsoXfD1sVuiK7fVBk1Fg |
| linkProvider | Scholars Portal |
| 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=PTOV1+promotes+cisplatin-induced+chemotherapy+resistance+by+activating+the+nuclear+factor+kappa+B+pathway+in+ovarian+cancer&rft.jtitle=Molecular+therapy.+Oncolytics&rft.au=Shen%2C+Hongwei&rft.au=Liao%2C+Bing&rft.au=Wan%2C+Zhiyong&rft.au=Zhao%2C+Yunhe&rft.date=2021-03-26&rft.pub=American+Society+of+Gene+%26+Cell+Therapy&rft.eissn=2372-7705&rft.volume=20&rft.spage=499&rft.epage=507&rft_id=info:doi/10.1016%2Fj.omto.2021.02.008&rft_id=info%3Apmid%2F33738336&rft.externalDocID=PMC7937561 |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2372-7705&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2372-7705&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2372-7705&client=summon |