Yigeng Feng, Hongwen Cao, Dan Wang, Lei Chen, Renjie Gao, Peng Sun
{"title":"JNK promotes the progression of castration-resistant prostate cancer.","authors":"Yigeng Feng, Hongwen Cao, Dan Wang, Lei Chen, Renjie Gao, Peng Sun","doi":"10.18388/abp.2020_6610","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Prostate cancer is one of the most common cancers in men worldwide. This study aims to elucidate the roles of c-Jun N-terminal kinase (JNK) in the progression of castration-resistant prostate cancer (CRPC).</p><p><strong>Methods: </strong>JNK overexpressing and knockdown cell lines were established on the PC-3 prostate cell line. qPCR and Western blotting were performed to determine the mRNA and protein levels of target genes in prostate tissues and cell lines. MTT and Matrigel invasion assays were conducted to evaluate the cell viability and invasive ability, respectively. The Kaplan-Meier estimator was performed to estimate the overall survival rate and second progression-free survival rate. Pearson's correlation coefficient was used to evaluate the relationship between JNK and prostate-specific antigen (PSA).</p><p><strong>Results: </strong>Relative JNK expression was correlated with Gleason score and PSA value in patients with CRPC. Kaplan-Meier analysis revealed that patients with low JNK expression exhibited high overall survival and second progression-free survival rate. In vitro assays demonstrated that JNK overexpression promoted cell viability and invasion as well as the protein expressions of extracellular signal-regulated kinase (ERK) and matrix metalloproteinase 1 (MMP1) in PC-3 cell lines.</p><p><strong>Conclusions: </strong>JNK overexpression promotes the development of CRPC via the regulation of ERK and MMP1.</p>","PeriodicalId":6984,"journal":{"name":"Acta biochimica Polonica","volume":"70 4","pages":"817-822"},"PeriodicalIF":1.4000,"publicationDate":"2023-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta biochimica Polonica","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.18388/abp.2020_6610","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Prostate cancer is one of the most common cancers in men worldwide. This study aims to elucidate the roles of c-Jun N-terminal kinase (JNK) in the progression of castration-resistant prostate cancer (CRPC).
Methods: JNK overexpressing and knockdown cell lines were established on the PC-3 prostate cell line. qPCR and Western blotting were performed to determine the mRNA and protein levels of target genes in prostate tissues and cell lines. MTT and Matrigel invasion assays were conducted to evaluate the cell viability and invasive ability, respectively. The Kaplan-Meier estimator was performed to estimate the overall survival rate and second progression-free survival rate. Pearson's correlation coefficient was used to evaluate the relationship between JNK and prostate-specific antigen (PSA).
Results: Relative JNK expression was correlated with Gleason score and PSA value in patients with CRPC. Kaplan-Meier analysis revealed that patients with low JNK expression exhibited high overall survival and second progression-free survival rate. In vitro assays demonstrated that JNK overexpression promoted cell viability and invasion as well as the protein expressions of extracellular signal-regulated kinase (ERK) and matrix metalloproteinase 1 (MMP1) in PC-3 cell lines.
Conclusions: JNK overexpression promotes the development of CRPC via the regulation of ERK and MMP1.
期刊介绍:
Acta Biochimica Polonica is a journal covering enzymology and metabolism, membranes and bioenergetics, gene structure and expression, protein, nucleic acid and carbohydrate structure and metabolism.