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Published on: September 8, 2017
Possible roles of vinexinbeta in growth and paclitaxel sensitivity in human prostate cancer PC-3 cells
Kosuke Mizutani1, Koh-ichi Nagata, Hidenori Ito
1Department of Urology, Gifu University Graduate School of Medicine, Gifu, Japan. islandminami@yahoo.co.jp
Purpose:
Vinexinbeta is an adaptor protein supposed to play pivotal roles in cell adhesion, cytoskeletal organization and signaling. Vinexinbeta is reported to be phosphorylated by extracelluler signal-regulated kinase (ERK) and the phosphorylation has been shown to be involved in cell adhesion, migration and growth. However, physiological function as well as pathophysiological relevance of vinexinbeta in cancer cells is almost unknown.
Methods:
By use of biochemical and cell biological techniques, we analyzed the effects of overexpression or RNAi-mediated silencing of vinexinbeta on the growth and paclitaxel sensitivity in a prostate cancer cell line PC-3.
Results:
Vinexinbeta was highly expressed in androgen-independent prostate cancer cell lines, PC-3 and DU145, but not in androgen-dependent LNCaP cells. We established two PC-3 cell lines, PC-3/Vinbeta#1 and #2, overexpressing GFP-tagged vinexinbeta and found that growth rate of these lines was significantly increased compared to a mock-transfected cell line. In addition, we found that PC-3/Vinbeta#1 and #2 became resistant to the treatment with 100 nM paclitaxel for 48 h. On the other hand, when siRNA-mediated vinexinbeta gene silencing was performed, PC-3 cell growth was suppressed. In addition, by vinexinbeta silencing, PC-3 cells became significantly sensitized to 10 nM paclitaxel treatment for 48 h.
Conclusions:
Vinexinbeta plays an important role in PC-3 cell growth, and abrogation of vinexinbeta may be effective for therapeutic cell death and enhanced chemotherapy sensitization in androgen-independent prostate cancer cells.
Insights
Vinexinbeta promotes prostate cancer cell growth and paclitaxel resistance. Silencing vinexinbeta inhibits growth and sensitizes cells to chemotherapy, suggesting therapeutic potential.
Area of Science:
- Molecular Biology
- Cancer Research
Background:
- Vinexinbeta is an adaptor protein involved in cell adhesion, cytoskeletal organization, and signaling.
- Phosphorylation of vinexinbeta by ERK impacts cell adhesion, migration, and growth.
- The role of vinexinbeta in cancer pathophysiology remains largely unexplored.
Purpose of the Study:
- To investigate the function of vinexinbeta in prostate cancer cell growth and response to paclitaxel.
- To analyze the effects of vinexinbeta overexpression and silencing on PC-3 cells.
Main Methods:
- Biochemical and cell biological techniques were employed.
- Prostate cancer cell line PC-3 was used to study vinexinbeta.
- Overexpression and RNAi-mediated silencing of vinexinbeta were performed.
Main Results:
- Vinexinbeta was highly expressed in androgen-independent PC-3 and DU145 cells, but not in LNCaP cells.
- Overexpression of vinexinbeta in PC-3 cells significantly increased growth rate and induced resistance to paclitaxel.
- Vinexinbeta gene silencing suppressed PC-3 cell growth and sensitized cells to paclitaxel.
Conclusions:
- Vinexinbeta plays a crucial role in the growth of PC-3 prostate cancer cells.
- Inhibiting vinexinbeta may induce therapeutic cell death in prostate cancer.
- Abrogating vinexinbeta can enhance chemotherapy sensitization in androgen-independent prostate cancer.
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