JNK promotes the progression of castration-resistant prostate cancer

被引:3
作者
Feng, Yigeng [1 ]
Cao, Hongwen [1 ]
Wang, Dan [1 ]
Chen, Lei [1 ]
Gao, Renjie [1 ]
Sun, Peng [1 ]
机构
[1] Shanghai Univ Tradit Chinese Med, Surg Dept 1, Urol Dept, LONGHUA Hosp, Shanghai 200032, Peoples R China
基金
中国国家自然科学基金;
关键词
Prostate cancer; PC3; prostate-specific antigen; castration; JNK; ANDROGEN DEPRIVATION THERAPY; MECHANISMS; PATHWAYS; STATISTICS; ILEXGENIN;
D O I
10.18388/abp.2020_6610
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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 progressionfree survival rate. In vitro assays demonstrated that JNK overexpression promoted cell viability and invasion as well as the protein expressions of extracellular signalregulated 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.
引用
收藏
页码:817 / 822
页数:6
相关论文
共 28 条
[1]   Targeting the PI3K/Akt/mTOR pathway in castration-resistant prostate cancer [J].
Bitting, Rhonda L. ;
Armstrong, Andrew J. .
ENDOCRINE-RELATED CANCER, 2013, 20 (03) :R83-R99
[2]   The functional contrariety of JNK [J].
Bode, Ann M. ;
Dong, Zigang .
MOLECULAR CARCINOGENESIS, 2007, 46 (08) :591-598
[3]   Mechanisms of resistance in castration-resistant prostate cancer (CRPC) [J].
Chandrasekar, Thenappan ;
Yang, Joy C. ;
Gao, Allen C. ;
Evans, Christopher P. .
TRANSLATIONAL ANDROLOGY AND UROLOGY, 2015, 4 (03) :365-380
[4]   Molecular mechanisms of castration-resistant prostate cancer progression [J].
Dutt, Smitha S. ;
Gao, Allen C. .
FUTURE ONCOLOGY, 2009, 5 (09) :1403-1413
[5]   Differential roles of ERK and Akt pathways in regulation of EGFR-mediated signaling and motility in prostate cancer cells [J].
Gan, Y. ;
Shi, C. ;
Inge, L. ;
Hibner, M. ;
Balducci, J. ;
Huang, Y. .
ONCOGENE, 2010, 29 (35) :4947-4958
[6]   The modern role of androgen deprivation therapy in the management of localised and locally advanced prostate cancer [J].
Gunner, Charlotte ;
Gulamhusein, Aziz ;
Rosario, Derek J. .
JOURNAL OF CLINICAL UROLOGY, 2016, 9 (02) :24-29
[7]   Androgen deprivation therapy: progress in understanding mechanisms of resistance and optimizing androgen depletion [J].
Harris, William P. ;
Mostaghel, Elahe A. ;
Nelson, Peter S. ;
Montgomery, Bruce .
NATURE CLINICAL PRACTICE UROLOGY, 2009, 6 (02) :76-85
[8]   Cotargeting Androgen Receptor Splice Variants and mTOR Signaling Pathway for the Treatment of Castration-Resistant Prostate Cancer [J].
Kato, Minoru ;
Banuelos, Carmen A. ;
Imamura, Yusuke ;
Leung, Jacky K. ;
Caley, Daniel P. ;
Wang, Jun ;
Mawji, Nasrin R. ;
Sadar, Marianne D. .
CLINICAL CANCER RESEARCH, 2016, 22 (11) :2744-2754
[9]  
Keyes M, 2013, CAN FAM PHYSICIAN, V59, P1269
[10]  
Kim Gyeong-Ji, 2018, Oncotarget, V9, P26370, DOI 10.18632/oncotarget.25316