CXCR4 promotes migration, invasion, and epithelial-mesenchymal transition of papillary thyroid carcinoma by activating STAT3 signaling pathway
ABSTRACT Aims: Papillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and leads to poor survival outcomes. The CXC chemokine receptor type 4 (CXCR4) plays an important role in many cellular movements such as transc...
Saved in:
| Published in | Journal of cancer research and therapeutics Vol. 20; no. 4; pp. 1241 - 1250 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
India
Wolters Kluwer - Medknow
01.08.2024
Medknow Publications and Media Pvt. Ltd Medknow Publications & Media Pvt. Ltd |
| Edition | 2 |
| Subjects | |
| Online Access | Get full text |
Cover
Loading…
| Abstract | ABSTRACT
Aims:
Papillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and leads to poor survival outcomes. The CXC chemokine receptor type 4 (CXCR4) plays an important role in many cellular movements such as transcriptional modulation, cell skeleton rearrangement, and cell migration, and the change in CXCR4 levels are crucial in various diseases including cancer. In this study, we explored the role of CXCR4 in the migration and invasion of PTC and investigated the potential mechanisms underlying its effects.
Subjects and Methods:
We analyzed the expression levels of CXCR4 in PTC tissues and cell lines. Would healing migration, Transwell invasion assay in vitro, and tail-vein lung metastasis assay In vivo were performed to evaluated the migration and invasion abilities of PTC cells with stable CXCR4 knockdown or overexpression. Signal transducers and activators of transcription (STAT3) signaling pathway-related protein expressions were examined by Western blotting assays.
Results:
The results showed that CXCR4 was highly expressed in PTC cell lines and PTC tissues. CXCR4 knockdown in PTC cells dampened the migration, invasion, and epithelial-mesenchymal transition (EMT), whereas CXCR4 overexpression enhanced these properties. In vivo, we also found that CXCR4 promoted the metastasis of PTC. Mechanistic studies showed that CXCR4 played these vital roles through the STAT3 signaling pathway. Furthermore, PTC patients with high CXCR4 or p-STAT3 expression correlated with aggressive clinical characteristics such as extrathyroidal extension (ETE), and lymph node metastasis (LNM).
Conclusions:
We provided evidence that CXCR4 might activate the STAT3 signaling pathway and further promote PTC development. Thus, CXCR4 might be a novel therapeutic target for PTC. |
|---|---|
| AbstractList | Papillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and leads to poor survival outcomes. The CXC chemokine receptor type 4 (CXCR4) plays an important role in many cellular movements such as transcriptional modulation, cell skeleton rearrangement, and cell migration, and the change in CXCR4 levels are crucial in various diseases including cancer. In this study, we explored the role of CXCR4 in the migration and invasion of PTC and investigated the potential mechanisms underlying its effects.AIMSPapillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and leads to poor survival outcomes. The CXC chemokine receptor type 4 (CXCR4) plays an important role in many cellular movements such as transcriptional modulation, cell skeleton rearrangement, and cell migration, and the change in CXCR4 levels are crucial in various diseases including cancer. In this study, we explored the role of CXCR4 in the migration and invasion of PTC and investigated the potential mechanisms underlying its effects.We analyzed the expression levels of CXCR4 in PTC tissues and cell lines. Would healing migration, Transwell invasion assay in vitro, and tail-vein lung metastasis assay In vivo were performed to evaluated the migration and invasion abilities of PTC cells with stable CXCR4 knockdown or overexpression. Signal transducers and activators of transcription (STAT3) signaling pathway-related protein expressions were examined by Western blotting assays.SUBJECTS AND METHODSWe analyzed the expression levels of CXCR4 in PTC tissues and cell lines. Would healing migration, Transwell invasion assay in vitro, and tail-vein lung metastasis assay In vivo were performed to evaluated the migration and invasion abilities of PTC cells with stable CXCR4 knockdown or overexpression. Signal transducers and activators of transcription (STAT3) signaling pathway-related protein expressions were examined by Western blotting assays.The results showed that CXCR4 was highly expressed in PTC cell lines and PTC tissues. CXCR4 knockdown in PTC cells dampened the migration, invasion, and epithelial-mesenchymal transition (EMT), whereas CXCR4 overexpression enhanced these properties. In vivo, we also found that CXCR4 promoted the metastasis of PTC. Mechanistic studies showed that CXCR4 played these vital roles through the STAT3 signaling pathway. Furthermore, PTC patients with high CXCR4 or p-STAT3 expression correlated with aggressive clinical characteristics such as extrathyroidal extension (ETE), and lymph node metastasis (LNM).RESULTSThe results showed that CXCR4 was highly expressed in PTC cell lines and PTC tissues. CXCR4 knockdown in PTC cells dampened the migration, invasion, and epithelial-mesenchymal transition (EMT), whereas CXCR4 overexpression enhanced these properties. In vivo, we also found that CXCR4 promoted the metastasis of PTC. Mechanistic studies showed that CXCR4 played these vital roles through the STAT3 signaling pathway. Furthermore, PTC patients with high CXCR4 or p-STAT3 expression correlated with aggressive clinical characteristics such as extrathyroidal extension (ETE), and lymph node metastasis (LNM).We provided evidence that CXCR4 might activate the STAT3 signaling pathway and further promote PTC development. Thus, CXCR4 might be a novel therapeutic target for PTC.CONCLUSIONSWe provided evidence that CXCR4 might activate the STAT3 signaling pathway and further promote PTC development. Thus, CXCR4 might be a novel therapeutic target for PTC. Papillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and leads to poor survival outcomes. The CXC chemokine receptor type 4 (CXCR4) plays an important role in many cellular movements such as transcriptional modulation, cell skeleton rearrangement, and cell migration, and the change in CXCR4 levels are crucial in various diseases including cancer. In this study, we explored the role of CXCR4 in the migration and invasion of PTC and investigated the potential mechanisms underlying its effects. We analyzed the expression levels of CXCR4 in PTC tissues and cell lines. Would healing migration, Transwell invasion assay in vitro, and tail-vein lung metastasis assay In vivo were performed to evaluated the migration and invasion abilities of PTC cells with stable CXCR4 knockdown or overexpression. Signal transducers and activators of transcription (STAT3) signaling pathway-related protein expressions were examined by Western blotting assays. The results showed that CXCR4 was highly expressed in PTC cell lines and PTC tissues. CXCR4 knockdown in PTC cells dampened the migration, invasion, and epithelial-mesenchymal transition (EMT), whereas CXCR4 overexpression enhanced these properties. In vivo, we also found that CXCR4 promoted the metastasis of PTC. Mechanistic studies showed that CXCR4 played these vital roles through the STAT3 signaling pathway. Furthermore, PTC patients with high CXCR4 or p-STAT3 expression correlated with aggressive clinical characteristics such as extrathyroidal extension (ETE), and lymph node metastasis (LNM). We provided evidence that CXCR4 might activate the STAT3 signaling pathway and further promote PTC development. Thus, CXCR4 might be a novel therapeutic target for PTC. Papillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and leads to poor survival outcomes. The CXC chemokine receptor type 4 (CXCR4) plays an important role in many cellular movements such as transcriptional modulation, cell skeleton rearrangement, and cell migration, and the change in CXCR4 levels are crucial in various diseases including cancer. In this study, we explored the role of CXCR4 in the migration and invasion of PTC and investigated the potential mechanisms underlying its effects. We analyzed the expression levels of CXCR4 in PTC tissues and cell lines. Would healing migration, Transwell invasion assay in vitro, and tail-vein lung metastasis assay In vivo were performed to evaluated the migration and invasion abilities of PTC cells with stable CXCR4 knockdown or overexpression. Signal transducers and activators of transcription (STAT3) signaling pathway-related protein expressions were examined by Western blotting assays. The results showed that CXCR4 was highly expressed in PTC cell lines and PTC tissues. CXCR4 knockdown in PTC cells dampened the migration, invasion, and epithelial-mesenchymal transition (EMT), whereas CXCR4 overexpression enhanced these properties. In vivo, we also found that CXCR4 promoted the metastasis of PTC. Mechanistic studies showed that CXCR4 played these vital roles through the STAT3 signaling pathway. Furthermore, PTC patients with high CXCR4 or p-STAT3 expression correlated with aggressive clinical characteristics such as extrathyroidal extension (ETE), and lymph node metastasis (LNM). We provided evidence that CXCR4 might activate the STAT3 signaling pathway and further promote PTC development. Thus, CXCR4 might be a novel therapeutic target for PTC. ABSTRACT Aims: Papillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and leads to poor survival outcomes. The CXC chemokine receptor type 4 (CXCR4) plays an important role in many cellular movements such as transcriptional modulation, cell skeleton rearrangement, and cell migration, and the change in CXCR4 levels are crucial in various diseases including cancer. In this study, we explored the role of CXCR4 in the migration and invasion of PTC and investigated the potential mechanisms underlying its effects. Subjects and Methods: We analyzed the expression levels of CXCR4 in PTC tissues and cell lines. Would healing migration, Transwell invasion assay in vitro, and tail-vein lung metastasis assay In vivo were performed to evaluated the migration and invasion abilities of PTC cells with stable CXCR4 knockdown or overexpression. Signal transducers and activators of transcription (STAT3) signaling pathway-related protein expressions were examined by Western blotting assays. Results: The results showed that CXCR4 was highly expressed in PTC cell lines and PTC tissues. CXCR4 knockdown in PTC cells dampened the migration, invasion, and epithelial-mesenchymal transition (EMT), whereas CXCR4 overexpression enhanced these properties. In vivo, we also found that CXCR4 promoted the metastasis of PTC. Mechanistic studies showed that CXCR4 played these vital roles through the STAT3 signaling pathway. Furthermore, PTC patients with high CXCR4 or p-STAT3 expression correlated with aggressive clinical characteristics such as extrathyroidal extension (ETE), and lymph node metastasis (LNM). Conclusions: We provided evidence that CXCR4 might activate the STAT3 signaling pathway and further promote PTC development. Thus, CXCR4 might be a novel therapeutic target for PTC. Keywords: CXCR4, invasion, migration, papillary thyroid cancer, STAT3 ABSTRACT Aims: Papillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and leads to poor survival outcomes. The CXC chemokine receptor type 4 (CXCR4) plays an important role in many cellular movements such as transcriptional modulation, cell skeleton rearrangement, and cell migration, and the change in CXCR4 levels are crucial in various diseases including cancer. In this study, we explored the role of CXCR4 in the migration and invasion of PTC and investigated the potential mechanisms underlying its effects. Subjects and Methods: We analyzed the expression levels of CXCR4 in PTC tissues and cell lines. Would healing migration, Transwell invasion assay in vitro, and tail-vein lung metastasis assay In vivo were performed to evaluated the migration and invasion abilities of PTC cells with stable CXCR4 knockdown or overexpression. Signal transducers and activators of transcription (STAT3) signaling pathway-related protein expressions were examined by Western blotting assays. Results: The results showed that CXCR4 was highly expressed in PTC cell lines and PTC tissues. CXCR4 knockdown in PTC cells dampened the migration, invasion, and epithelial-mesenchymal transition (EMT), whereas CXCR4 overexpression enhanced these properties. In vivo, we also found that CXCR4 promoted the metastasis of PTC. Mechanistic studies showed that CXCR4 played these vital roles through the STAT3 signaling pathway. Furthermore, PTC patients with high CXCR4 or p-STAT3 expression correlated with aggressive clinical characteristics such as extrathyroidal extension (ETE), and lymph node metastasis (LNM). Conclusions: We provided evidence that CXCR4 might activate the STAT3 signaling pathway and further promote PTC development. Thus, CXCR4 might be a novel therapeutic target for PTC. ABSTRACTAims:Papillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and leads to poor survival outcomes. The CXC chemokine receptor type 4 (CXCR4) plays an important role in many cellular movements such as transcriptional modulation, cell skeleton rearrangement, and cell migration, and the change in CXCR4 levels are crucial in various diseases including cancer. In this study, we explored the role of CXCR4 in the migration and invasion of PTC and investigated the potential mechanisms underlying its effects.Subjects and Methods:We analyzed the expression levels of CXCR4 in PTC tissues and cell lines. Would healing migration, Transwell invasion assay in vitro, and tail-vein lung metastasis assay In vivo were performed to evaluated the migration and invasion abilities of PTC cells with stable CXCR4 knockdown or overexpression. Signal transducers and activators of transcription (STAT3) signaling pathway-related protein expressions were examined by Western blotting assays.Results:The results showed that CXCR4 was highly expressed in PTC cell lines and PTC tissues. CXCR4 knockdown in PTC cells dampened the migration, invasion, and epithelial-mesenchymal transition (EMT), whereas CXCR4 overexpression enhanced these properties. In vivo, we also found that CXCR4 promoted the metastasis of PTC. Mechanistic studies showed that CXCR4 played these vital roles through the STAT3 signaling pathway. Furthermore, PTC patients with high CXCR4 or p-STAT3 expression correlated with aggressive clinical characteristics such as extrathyroidal extension (ETE), and lymph node metastasis (LNM).Conclusions:We provided evidence that CXCR4 might activate the STAT3 signaling pathway and further promote PTC development. Thus, CXCR4 might be a novel therapeutic target for PTC. |
| Audience | Professional |
| Author | Liu, Bin Xu, Zhipeng Hu, Yajie Hou, Haitao Wei, Dan Tang, Yuanqi Hu, Wenxin Zhou, Dongsheng Long, Houlong Zhao, Quanlin Wang, Jianning |
| Author_xml | – sequence: 1 givenname: Yajie surname: Hu fullname: Hu, Yajie – sequence: 2 givenname: Zhipeng surname: Xu fullname: Xu, Zhipeng – sequence: 3 givenname: Dongsheng surname: Zhou fullname: Zhou, Dongsheng – sequence: 4 givenname: Haitao surname: Hou fullname: Hou, Haitao – sequence: 5 givenname: Bin surname: Liu fullname: Liu, Bin – sequence: 6 givenname: Houlong surname: Long fullname: Long, Houlong – sequence: 7 givenname: Wenxin surname: Hu fullname: Hu, Wenxin – sequence: 8 givenname: Yuanqi surname: Tang fullname: Tang, Yuanqi – sequence: 9 givenname: Jianning surname: Wang fullname: Wang, Jianning – sequence: 10 givenname: Dan surname: Wei fullname: Wei, Dan email: 77weidan@163.com – sequence: 11 givenname: Quanlin surname: Zhao fullname: Zhao, Quanlin email: 18516188617@163.com |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/39206986$$D View this record in MEDLINE/PubMed |
| BookMark | eNp9ksuK2zAUhk2Z0slM-wDdFEE3XdSprra1DGF6Y6DQptCdkBUpUUaWXMmekJfoM1dJZnoZ0iKwbPP9h_-c818UZz54XRTPEZxSBMmbjYrDdP8QmHAmMH5UTBDnTUkRac6KCeQ1KRFt8HlxkdIGQlZj3DwpzgnHsOJNNSl-zL_NP1PQx9CFQSfQ2VWUgw3-NbD-VqbDm_RLoHs7rLWz0pWdTtqr9a6TDgxR-mT3AhAM6GVvnZNxB4b1Lga7BEpGZX3oJGh3QKrB3ubqfgW-LGYLApJdeen2370c1lu5e1o8NtIl_ezuviy-vr1azN-X15_efZjPrkvFKE1lDau2rSk3RhFqGDScEaWhkQYzyiiHhKmqpUSRumlIxWhL24pQktuXaElaclm8OtbNjX8fdRpEZ5PS2bvXYUyCQM7rPCBWZfTlA3QTxphtZwqhPF2OMPpNraTTwnoT8mTUvqiYNajBkKGaZKo8Qa2011G6vFtj8--_-OkJPp-l7qw6KXhxZ3ZsO70UfbRdXoe4X3gG0BFQMaQUtfmFICj2oRKHPP0ZqqypH2iUHQ4hyW6s-6_y41G5DW7QMd24caujyM5ufNj-WygQpkgcoinuo0l-AqFC7ds |
| CitedBy_id | crossref_primary_10_4103_jcrt_jcrt_933_24 |
| Cites_doi | 10.1507/endocrj.EJ21-0076 10.1016/j.canlet.2014.08.012 10.1073/pnas.2013319117 10.1002/cbin.10794 10.4103/jcrt.jcrt_188_22 10.4103/jcrt.jcrt_212_22 10.3390/cancers13215567 10.4103/jcrt.jcrt_1737_21 10.1016/j.canlet.2020.12.026 10.1158/0008-5472.CAN-17-2158 10.7150/thno.54027 10.1158/2326-6066.CIR-19-1005 10.1016/j.jid.2020.06.034 10.1186/s12943-020-01294-3 10.1016/j.ymthe.2020.09.034 10.1016/j.semcancer.2019.09.022 10.1038/s41388-018-0519-2 10.1038/s41375-021-01376-1 10.21037/atm-20-1054 10.1016/j.canlet.2020.02.026 10.1089/thy.2019.0229 10.3389/fcell.2021.687322 10.1007/s13277-013-0725-z 10.1158/0008-5472.CAN-17-3131 10.1073/pnas.2015433118 10.3390/ijms16036153 10.1038/nrendo.2016.224 10.1186/s13046-014-0103-8 10.1089/thy.2018.0609 10.1038/s41467-020-18497-3 10.4103/jcrt.JCRT_480_19 10.1182/blood-2017-04-776740 10.4103/jcrt.jcrt_1471_22 10.1038/onc.2017.108 10.1158/0008-5472.CAN-18-0620 10.1016/j.ccell.2016.03.004 10.1146/annurev-pharmtox-010919-023340 10.4103/jcrt.JCRT_1268_20 10.1186/s12943-020-01258-7 |
| ContentType | Journal Article |
| Copyright | Copyright: © 2024 Journal of Cancer Research and Therapeutics Copyright © 2024 Copyright: © 2024 Journal of Cancer Research and Therapeutics. COPYRIGHT 2024 Medknow Publications and Media Pvt. Ltd. 2024. This article is published under (http://creativecommons.org/licenses/by-nc-sa/3.0/) (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
| Copyright_xml | – notice: Copyright: © 2024 Journal of Cancer Research and Therapeutics – notice: Copyright © 2024 Copyright: © 2024 Journal of Cancer Research and Therapeutics. – notice: COPYRIGHT 2024 Medknow Publications and Media Pvt. Ltd. – notice: 2024. This article is published under (http://creativecommons.org/licenses/by-nc-sa/3.0/) (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
| DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM K9. 7X8 |
| DOI | 10.4103/jcrt.jcrt_2395_22 |
| DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed ProQuest Health & Medical Complete (Alumni) MEDLINE - Academic |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) ProQuest Health & Medical Complete (Alumni) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE - Academic MEDLINE ProQuest Health & Medical Complete (Alumni) |
| Database_xml | – sequence: 1 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: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine Pharmacy, Therapeutics, & Pharmacology |
| EISSN | 1998-4138 |
| Edition | 2 |
| EndPage | 1250 |
| ExternalDocumentID | A818205173 39206986 10_4103_jcrt_jcrt_2395_22 JCRAT-20-1241 |
| Genre | Journal Article |
| GeographicLocations | China |
| GeographicLocations_xml | – name: China |
| GroupedDBID | --- 29K 2WC 53G 5GY 5VS 7X7 88E 8FI 8FJ 8G5 AAWTL ABDBF ABJNI ABUWG ABVJJ ACGFS ACUHS ADBBV AENEX AFKRA AHMBA ALIPV ALMA_UNASSIGNED_HOLDINGS AZQEC BAWUL BCNDV BENPR BPHCQ BVXVI CCPQU D-I DIK DU5 DWQXO E3Z EBD EBS EJD EMOBN EOJEC ESX F5P FYUFA GNUQQ GUQSH GX1 H13 HMCUK IAO IEA IHE IHR IL9 INH INR IOF IPNFZ IPO ITC KQ8 M1P M2O M48 OBODZ OK1 OVD P2P P6G PHGZM PHGZT PIMPY PMFND PQQKQ PROAC PSQYO RBI RIG RMW RNS SV3 TEORI TR2 TUS UKHRP W3E XSB ~8M AAYXX ADJBI CITATION OVT 3V. CGR CUY CVF ECM EIF GROUPED_DOAJ M~E NPM K9. 7X8 |
| ID | FETCH-LOGICAL-c544s-706bb749ffc34f50f953ce0faf254549035c6b43c37883654b4b6343722a1d3b3 |
| IEDL.DBID | W3E |
| ISSN | 0973-1482 1998-4138 |
| IngestDate | Fri Jul 11 04:23:55 EDT 2025 Mon Jun 30 12:17:44 EDT 2025 Tue Jun 17 22:01:25 EDT 2025 Fri Jun 13 00:00:02 EDT 2025 Tue Jun 10 21:01:05 EDT 2025 Wed Feb 19 02:07:37 EST 2025 Tue Jul 01 01:29:20 EDT 2025 Thu Apr 24 23:11:56 EDT 2025 Wed May 28 23:12:50 EDT 2025 |
| IsDoiOpenAccess | true |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 4 |
| Keywords | migration CXCR4 invasion papillary thyroid cancer STAT3 |
| Language | English |
| License | Copyright © 2024 Copyright: © 2024 Journal of Cancer Research and Therapeutics. |
| LinkModel | DirectLink |
| MergedId | FETCHMERGED-LOGICAL-c544s-706bb749ffc34f50f953ce0faf254549035c6b43c37883654b4b6343722a1d3b3 |
| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
| OpenAccessLink | https://doi.org/10.4103/jcrt.jcrt_2395_22 |
| PMID | 39206986 |
| PQID | 3111489121 |
| PQPubID | 226490 |
| PageCount | 10 |
| ParticipantIDs | proquest_miscellaneous_3099798656 proquest_journals_3111489121 gale_infotracmisc_A818205173 gale_infotracgeneralonefile_A818205173 gale_infotracacademiconefile_A818205173 pubmed_primary_39206986 crossref_primary_10_4103_jcrt_jcrt_2395_22 crossref_citationtrail_10_4103_jcrt_jcrt_2395_22 wolterskluwer_medknow_10_4103_jcrt_jcrt_2395_22_1241_CXCR4_promotes |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 20240800 2024-08-00 2024-Aug-01 20240801 |
| PublicationDateYYYYMMDD | 2024-08-01 |
| PublicationDate_xml | – month: 08 year: 2024 text: 20240800 |
| PublicationDecade | 2020 |
| PublicationPlace | India |
| PublicationPlace_xml | – name: India – name: Mumbai |
| PublicationTitle | Journal of cancer research and therapeutics |
| PublicationTitleAlternate | J Cancer Res Ther |
| PublicationYear | 2024 |
| Publisher | Wolters Kluwer - Medknow Medknow Publications and Media Pvt. Ltd Medknow Publications & Media Pvt. Ltd |
| Publisher_xml | – name: Wolters Kluwer - Medknow – name: Medknow Publications and Media Pvt. Ltd – name: Medknow Publications & Media Pvt. Ltd |
| References | Buch (R16-20241021) 2023; 19 Qu (R15-20241021) 2016; 29 Cave (R27-20241021) 2021; 11 Jain (R6-20241021) 2020; 30 Zhang (R39-20241021) 2017; 41 Yu (R7-20241021) 2020; 11 Dai (R17-20241021) 2022; 18 Thilakasiri (R35-20241021) 2021; 68 He (R38-20241021) 2018; 78 Bhat (R22-20241021) 2021; 20 Boruah (R19-20241021) 2023; 19 Song (R10-20241021) 2019; 38 Qin (R37-20241021) 2020; 476 Bronte (R23-20241021) 2020; 8 Sun (R28-20241021) 2021; 29 Patricia (R29-20241021) 2017; 130 Hu (R33-20241021) 2014; 354 Brito (R2-20241021) 2017; 13 Cai (R32-20241021) 2020; 8 Cao (R14-20241021) 2022; 69 Ulisse (R18-20241021) 2021; 13 Grant (R20-20241021) 2015; 4 Aronovich (R26-20241021) 2021; 141 Yin (R30-20241021) 2021; 9 Lewis (R12-20241021) 2021; 35 Zhao (R31-20241021) 2014; 33 Zou (R36-20241021) 2020; 19 Oh (R1-20241021) 2019; 29 Elaziz (R8-20241021) 2021; 17 Smit (R25-20241021) 2021; 61 Valeta-Magara (R24-20241021) 2019; 79 Fallahi (R21-20241021) 2015; 16 Song (R11-20241021) 2021; 118 Yang (R34-20241021) 2019; 79 Shen (R40-20241021) 2013; 34 Melik (R4-20241021) 2022; 18 Pan (R3-20241021) 2021; 501 Devi (R5-20241021) 2023; 19 Işbilir (R9-20241021) 2020; 117 Xiang (R13-20241021) 2017; 36 |
| References_xml | – volume: 69 start-page: 189 year: 2022 ident: R14-20241021 article-title: Expression of CXCR4 and CXCR7 in papillary thyroid carcinoma and adjacent tissues and their relationship with pathologic indicators of tumor aggressiveness publication-title: Endocr J doi: 10.1507/endocrj.EJ21-0076 – volume: 354 start-page: 417 year: 2014 ident: R33-20241021 article-title: SDF-1/CXCR4 promotes epithelial-mesenchymal transition and progression of colorectal cancer by activation of the Wnt/?-catenin signaling pathway publication-title: Cancer Lett doi: 10.1016/j.canlet.2014.08.012 – volume: 117 start-page: 29144 year: 2020 ident: R9-20241021 article-title: Advanced fluorescence microscopy reveals disruption of dynamic CXCR4 dimerization by subpocket-specific inverse agonists publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.2013319117 – volume: 41 start-page: 854 year: 2017 ident: R39-20241021 article-title: C-X-C motif chemokine receptor 4 promotes tumor angiogenesis in gastric cancer via activation of JAK2/STAT3 publication-title: Cell Biol Int doi: 10.1002/cbin.10794 – volume: 19 start-page: 1697 year: 2023 ident: R16-20241021 article-title: Tumor budding in breast carcinoma:A systematic review and meta-analysis publication-title: J Cancer Res Ther doi: 10.4103/jcrt.jcrt_188_22 – volume: 18 start-page: 1328 year: 2022 ident: R17-20241021 article-title: Effects of the CRYAB gene on stem cell-like properties of colorectal cancer and its mechanism publication-title: J J Cancer Res Ther doi: 10.4103/jcrt.jcrt_212_22 – volume: 13 start-page: 5567 year: 2021 ident: R18-20241021 article-title: Papillary thyroid cancer prognosis:An evolving field publication-title: Cancers doi: 10.3390/cancers13215567 – volume: 19 start-page: 2094 year: 2023 ident: R5-20241021 article-title: Mandibular metastasis of follicular thyroid carcinoma publication-title: J Cancer Res Ther doi: 10.4103/jcrt.jcrt_1737_21 – volume: 501 start-page: 31 year: 2021 ident: R3-20241021 article-title: HN1 promotes tumor growth and metastasis of anaplastic thyroid carcinoma by interacting with STMN1 publication-title: Cancer Lett doi: 10.1016/j.canlet.2020.12.026 – volume: 79 start-page: 3360 year: 2019 ident: R24-20241021 article-title: Inflammatory breast cancer promotes development of M2 tumor-associated macrophages and cancer mesenchymal cells through a complex chemokine network publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-17-2158 – volume: 4 start-page: 52 year: 2015 ident: R20-20241021 article-title: Recurrence of papillary thyroid cancer after optimized surgery publication-title: Gland Surg – volume: 11 start-page: 5686 year: 2021 ident: R27-20241021 article-title: Nodal-induced L1CAM/CXCR4 subpopulation sustains tumor growth and metastasis in colorectal cancer derived organoids publication-title: Theranostics doi: 10.7150/thno.54027 – volume: 8 start-page: 160 year: 2020 ident: R23-20241021 article-title: Macrophages instruct aberrant glycosylation in colon cancer by chemokine and cytokine signals publication-title: Cancer Immunol Res doi: 10.1158/2326-6066.CIR-19-1005 – volume: 141 start-page: 619 year: 2021 ident: R26-20241021 article-title: Cancer-associated fibroblasts in mycosis fungoides promote tumor cell migration and drug resistance through CXCL12/CXCR4 publication-title: J Invest Dermatol doi: 10.1016/j.jid.2020.06.034 – volume: 20 start-page: 2 year: 2021 ident: R22-20241021 article-title: Cytokine-chemokine network driven metastasis in esophageal cancer;Promising avenue for targeted therapy publication-title: Mol Cancer doi: 10.1186/s12943-020-01294-3 – volume: 29 start-page: 60 year: 2021 ident: R28-20241021 article-title: Olaparib suppresses MDSC recruitment via SDF1?/CXCR4 axis to improve the anti-tumor efficacy of CAR-T cells on breast cancer in mice publication-title: Mol Ther doi: 10.1016/j.ymthe.2020.09.034 – volume: 68 start-page: 31 year: 2021 ident: R35-20241021 article-title: Repurposing of drugs as STAT3 inhibitors for cancer therapy publication-title: Semin Cancer Biol doi: 10.1016/j.semcancer.2019.09.022 – volume: 38 start-page: 1560 year: 2019 ident: R10-20241021 article-title: CXCR7/CXCR4 heterodimer-induced histone demethylation:A new mechanism of colorectal tumorigenesis publication-title: Oncogene doi: 10.1038/s41388-018-0519-2 – volume: 35 start-page: 2895 year: 2021 ident: R12-20241021 article-title: CXCR4 hyperactivation cooperates with TCL1 in CLL development and aggressiveness publication-title: Leukemia doi: 10.1038/s41375-021-01376-1 – volume: 8 start-page: 929 year: 2020 ident: R32-20241021 article-title: Extracellular ubiquitin promotes hepatoma metastasis by mediating M2 macrophage polarization via the activation of the CXCR4/ERK signaling pathway publication-title: Ann Transl Med doi: 10.21037/atm-20-1054 – volume: 476 start-page: 161 year: 2020 ident: R37-20241021 article-title: Laminin 521 enhances self-renewal via STAT3 activation and promotes tumor progression in colorectal cancer publication-title: Cancer Lett doi: 10.1016/j.canlet.2020.02.026 – volume: 30 start-page: 1037 year: 2020 ident: R6-20241021 article-title: Extrathyroidal extension is an important predictor of regional lymph node metastasis in pediatric differentiated thyroid cancer publication-title: Thyroid doi: 10.1089/thy.2019.0229 – volume: 9 start-page: 687322 year: 2021 ident: R30-20241021 article-title: CD44v6-O-MWNTS-Loaded Gemcitabine and CXCR4 siRNA Improves the Anti-tumor effectiveness of ovarian cancer publication-title: Front Cell Dev Biol doi: 10.3389/fcell.2021.687322 – volume: 34 start-page: 1839 year: 2013 ident: R40-20241021 article-title: CXCR4-mediated Stat3 activation is essential for CXCL12-induced cell invasion in bladder cancer publication-title: Tumour Biol doi: 10.1007/s13277-013-0725-z – volume: 78 start-page: 3293 year: 2018 ident: R38-20241021 article-title: IL22RA1/STAT3 signaling promotes stemness and tumorigenicity in pancreatic cancer publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-17-3131 – volume: 118 start-page: e2015433118 year: 2021 ident: R11-20241021 article-title: A highly selective and potent CXCR4 antagonist for hepatocellular carcinoma treatment publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.2015433118 – volume: 16 start-page: 6153 year: 2015 ident: R21-20241021 article-title: New therapies for dedifferentiated papillary thyroid cancer publication-title: Int J Mol Sci doi: 10.3390/ijms16036153 – volume: 13 start-page: 131 year: 2017 ident: R2-20241021 article-title: Thyroid cancer:Overdiagnosis of papillary carcinoma-who benefits? publication-title: Nat Rev Endocrinol doi: 10.1038/nrendo.2016.224 – volume: 33 start-page: 103 year: 2014 ident: R31-20241021 article-title: Blockade of CXCL12/CXCR4 signaling inhibits intrahepatic cholangiocarcinoma progression and metastasis via inactivation of canonical Wnt pathway publication-title: J Exp Clin Cancer Res doi: 10.1186/s13046-014-0103-8 – volume: 29 start-page: 642 year: 2019 ident: R1-20241021 article-title: Tumor volume doubling time in active surveillance of papillary thyroid carcinoma publication-title: Thyroid doi: 10.1089/thy.2018.0609 – volume: 11 start-page: 4807 year: 2020 ident: R7-20241021 article-title: Lymph node metastasis prediction of papillary thyroid carcinoma based on transfer learning radiomics publication-title: Nat Commun doi: 10.1038/s41467-020-18497-3 – volume: 17 start-page: 1454 year: 2021 ident: R8-20241021 article-title: CXCR4 and RIF1 overexpression induces resistance of epithelial ovarian cancer to cisplatin-based chemotherapy publication-title: J Cancer Res Ther doi: 10.4103/jcrt.JCRT_480_19 – volume: 130 start-page: 501 year: 2017 ident: R29-20241021 article-title: SOX11 promotes tumor protective microenvironment interactions through CXCR4 and FAK regulation in mantle cell lymphoma publication-title: Blood doi: 10.1182/blood-2017-04-776740 – volume: 19 start-page: 312 year: 2023 ident: R19-20241021 article-title: PD-L1 expression in rare and aggressive thyroid cancers:A preliminary investigation for a role of immunotherapy publication-title: J Cancer Res Ther doi: 10.4103/jcrt.jcrt_1471_22 – volume: 36 start-page: 5122 year: 2017 ident: R13-20241021 article-title: A positive crosstalk between CXCR4 and CXCR2 promotes gastric cancer metastasis publication-title: Oncogene doi: 10.1038/onc.2017.108 – volume: 79 start-page: 735 year: 2019 ident: R34-20241021 article-title: Inhibition of dipeptidyl peptidase-4 accelerates epithelial-mesenchymal transition and breast cancer metastasis via the CXCL12/CXCR4/mTOR axis publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-18-0620 – volume: 29 start-page: 653 year: 2016 ident: R15-20241021 article-title: Exosome-transmitted lncARSR promotes sunitinib resistance in renal cancer by acting as a competing endogenous RNA publication-title: Cancer Cell doi: 10.1016/j.ccell.2016.03.004 – volume: 61 start-page: 541 year: 2021 ident: R25-20241021 article-title: The CXCL12/CXCR4/ACKR3 Axis in the tumor microenvironment:Signaling, crosstalk, and therapeutic targeting publication-title: Annu Rev Pharmacol Toxicol doi: 10.1146/annurev-pharmtox-010919-023340 – volume: 18 start-page: 1042 year: 2022 ident: R4-20241021 article-title: Assessment of preoperative thyroglobulin levels in papillary thyroid cancer publication-title: J Cancer Res Ther doi: 10.4103/jcrt.JCRT_1268_20 – volume: 19 start-page: 145 year: 2020 ident: R36-20241021 article-title: Targeting STAT3 in cancer immunotherapy publication-title: Mol Cancer doi: 10.1186/s12943-020-01258-7 |
| SSID | ssj0057228 |
| Score | 2.3331351 |
| Snippet | ABSTRACT
Aims:
Papillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and... Papillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and leads to poor... ABSTRACT Aims: Papillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and... ABSTRACTAims:Papillary thyroid cancer (PTC) is a serious threat to human health worldwide, while metastasis in the early phase limits therapeutic success and... |
| SourceID | proquest gale pubmed crossref wolterskluwer |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 1241 |
| SubjectTerms | Animals Cell Line, Tumor Cell Movement Cell Proliferation Development and progression Epithelial-Mesenchymal Transition Female Gene Expression Regulation, Neoplastic Humans Lung cancer Male Metastasis Mice Middle Aged Neoplasm Invasiveness Original Article Receptors, CXCR4 - genetics Receptors, CXCR4 - metabolism Signal Transduction STAT3 Transcription Factor - genetics STAT3 Transcription Factor - metabolism Thyroid cancer Thyroid Cancer, Papillary - genetics Thyroid Cancer, Papillary - metabolism Thyroid Cancer, Papillary - pathology Thyroid Neoplasms - genetics Thyroid Neoplasms - metabolism Thyroid Neoplasms - pathology Xenograft Model Antitumor Assays |
| Title | CXCR4 promotes migration, invasion, and epithelial-mesenchymal transition of papillary thyroid carcinoma by activating STAT3 signaling pathway |
| URI | https://doi.org/10.4103/jcrt.jcrt_2395_22 https://www.ncbi.nlm.nih.gov/pubmed/39206986 https://www.proquest.com/docview/3111489121 https://www.proquest.com/docview/3099798656 |
| Volume | 20 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1fa9swEBejgzEYY-v-ueuGBiODETPbkiz7MYSWMugoW8ryJiRZTrM1dojTFn-Jfebd2U4aj25PezEGnYXtO-nudHe_I-S9tCyJM7DcXJxan2eR8Y1MM9-hdo0T6UKL55CnX-KTc_55KqYdWDTWwuzE73kYsE8_7ApMNLioiKVCRbDb3o9kJDB76zs72my6QkZNG1UEn_ER2rINYN49RU8F_bkR72iiRzclRqyrn03C-o7aOX5CHnf2Ih21DH5K7rlinzw47SLi-2Rw1mJP10M6uS2lqoZ0QM9uUanrZ-TXeDr-yumySb9zFV3MZy3zh3ReXOuqudNFRt0SyzQuQS79BZYm2Yt6AW-wRqXW5HfRMqdLvcR2RauaAqNX5TyjFpsSFeVCU1NTrJbAs95iRr9NRhNGMU1EY-U7xRbIN7p-Ts6PjybjE79rxuBbwXnlyyA2RvI0zy3juQjyVDDrglzn4GKCkxkwYWPDmUWAehYLbriJGUYFIx1mzLAXZK8oC_eKUJ66XMuEMSlynjFwqnQYIUo4s9Jom3kk2PBH2Q6pHBtmXCrwWJClquHmLks98nH7yLKF6fgX8QdkusIlDPNa3VUiwNshGJYaJYhqL0LJPDLoUc5aKPC7CA97hLBGbX94I1-q2yMqxUL0RdMwCj3ybjuMT2LeW-HKK6DBwuY0AaPbIy9budx-H1i2QQxjHhn3BFUt2kLKv_8ABUZdqBqxUxuxO_gvs7wmDyOw-toMyUOyt15duTdgta3N22a9_ga1tkNG |
| linkProvider | Wolters Kluwer Health |
| 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=CXCR4+promotes+migration%2C+invasion%2C+and+epithelial-mesenchymal+transition+of+papillary+thyroid+carcinoma+by+activating+STAT3+signaling+pathway&rft.jtitle=Journal+of+cancer+research+and+therapeutics&rft.au=Hu%2C+Yajie&rft.au=Xu%2C+Zhipeng&rft.au=Zhou%2C+Dongsheng&rft.au=Hou%2C+Haitao&rft.date=2024-08-01&rft.issn=1998-4138&rft.eissn=1998-4138&rft.volume=20&rft.issue=4&rft.spage=1241&rft_id=info:doi/10.4103%2Fjcrt.jcrt_2395_22&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0973-1482&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0973-1482&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0973-1482&client=summon |