TAZ is overexpressed in prostate cancers and regulates the proliferation, migration and apoptosis of prostate cancer PC3 cells

Lin,Mengyuan; Bu,Chaozhi; He,Qingwen; Gu,Jiayu; Wang,Honghua; Feng,Ninghan; Jiang,Shi‑Wen

doi:10.3892/or.2020.7616

TAZ is overexpressed in prostate cancers and regulates the proliferation, migration and apoptosis of prostate cancer PC3 cells

Authors:
- Mengyuan Lin
- Chaozhi Bu
- Qingwen He
- Jiayu Gu
- Honghua Wang
- Ninghan Feng
- Shi‑Wen Jiang
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Affiliations: Joint Laboratory of SKLRM (State Key Laboratory of Reproductive Medicine), The Affiliated Wuxi Maternity and Child Health Care Hospital of Nanjing Medical University, Wuxi, Jiangsu 214002, P.R. China, Department of Urology, The Affiliated Wuxi No. 2 People's Hospital of Nanjing Medical University, Wuxi, Jiangsu 214002, P.R. China
Published online on: May 19, 2020 https://doi.org/10.3892/or.2020.7616
Pages: 747-756

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Abstract

TAZ (transcriptional coactivator with PDZ‑binding motif), which is also known as WW domain‑containing transcription regulator 1 (WWTR1), a downstream effector of the Hippo pathway, has been reported to regulate cancer cell proliferation, migration and apoptosis by acting as a transcriptional coactivator. However, the function of TAZ in prostate cancer cells has not been investigated. In the present study, TAZ expression in prostate cancer (PCa) and benign prostatic hyperplasia tissues, PCa cell lines, and normal prostate epithelial cells was determined with the use of immunohistochemistry. TAZ was knocked down by shRNA in the PC3 cells, a prostate cancer cell line, and cell viability and migration assays were performed to determine the biological functions of TAZ. A mouse subcutaneous xenograft model was used to determine the in vivo effects of TAZ knockdown on tumor growth. We demonstrated that TAZ is overexpressed in PCa tissues, and the expression levels were found to be positively correlated with the Gleason scores of cancer grade. Moreover, TAZ knockdown inhibited PC3 cell proliferation, reduced cell migration, and induced apoptosis. Further experiments demonstrated that TAZ knockdown may lead to PC3 cell apoptosis through the exogenous apoptotic pathway by inducing the expression and cleavage of caspase‑4 and ‑7. In the tumor xenograft model, TAZ knockdown led to a decreased tumor growth rate. Taken together, the experimental results indicate that TAZ plays a significant role in the proliferation, migration and apoptosis of prostate cancer cells. TAZ could be a useful biomarker for PCa diagnosis/prognosis, and it could be a potential target for the treatment of prostate cancers.

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