Caveolin-1 and -2 regulate cell motility in castration-resistant prostate cancer

• Published in: Research and reports in urology Vol. 10; pp. 135 - 144
• Main Authors: Kamibeppu, Toyoharu, Yamasaki, Koji, Nakahara, Kozue, Nagai, Takahiro, Terada, Naoki, Tsukino, Hiromasa, Mukai, Shoichiro, Kamoto, Toshiyuki
• Format: Journal Article
• Language: English
• Published: England Taylor & Francis Ltd 01.01.2018; Dove Medical Press
• Subjects: Adipocytes; Androgens; Binding sites; Breast cancer; Cancer therapies; Caveolin-2; Cell adhesion & migration; Cell culture; cell motility; Cervical cancer; CRPC; Cvaolin-1; Esophagus; Gastric cancer; Gene expression; Growth factors; Homeostasis; Kinases; Lung cancer; Metastasis; Original Research; Physiology; Prostate cancer; Proteins; Signal transduction; Smooth muscle; United States > US; Japan; cell motility; caveolin-1; CRPC; caveolin-2
• ISSN: 2253-2447; 2253-2447
• DOI: 10.2147/RRU.S173377

Caveolin (Cav)-1 and Cav-2 are cell membrane proteins, which are structural proteins of caveolae and are reported to be positive regulators of cell survival and metastasis in prostate cancer (PC). In a previous study, we reported that elevated levels of Cav-1 and Cav-2 were significantly associated with PC progression. However, their functions in PC have not yet been clarified. In this study, we examined the function of Cav-1 and Cav-2 in PC cell invasiveness and motility. We introduced Cav-1- and Cav-2-specific small interfering into PC3 cells to knock-down (KD) both molecules. We also performed cell proliferation assay, wound healing assay, migration assay, and invasion assay using PC3 cells and compared the results between Cav-1-KD, Cav-2-KD, and negative control PC3 cells. In addition, we performed real-time quantitative PCR (RT-qPCR) and RT2 Profiler PCR Array analysis to identify factors influencing migration. We observed no significant difference in the proliferative and invasive activities of Cav-1-KD and Cav-2-KD PC3 cells; however, the cell motility was significantly decreased compared with negative control PC3 cells. RT-qPCR revealed that the expression of vimentin and N-cadherin was downregulated in Cav-1-KD PC3 cells. In addition, PCR array revealed a decreased expression of MGAT5, MMP13, and MYCL in Cav-1-KD PC3 and ETV4, FGFR4, and SRC in Cav-2-KD PC3. Cav-1 and Cav-2 may positively contribute to the upregulation of castration-resistant PC cell migration. Cav-induced regulation of several molecules including vimentin, N-cadherin, MGAT5, MMP13, MYCL, ETV4, FGFR4, and SRC may have an important role in PC3 cell motility. However, further examination will be required.