Receptor-like protein tyrosine phosphatase κ negatively regulates the apoptosis of prostate cancer cells via the JNK pathway

Sun, Ping-Hui, Ye, Lin ORCID: https://orcid.org/0000-0002-0303-2409, Mason, Malcolm David ORCID: https://orcid.org/0000-0003-1505-2869 and Jiang, Wen Guo ORCID: https://orcid.org/0000-0002-3283-1111 2013. Receptor-like protein tyrosine phosphatase κ negatively regulates the apoptosis of prostate cancer cells via the JNK pathway. International Journal of Oncology 43 (5) , pp. 1560-1568. 10.3892/ijo.2013.2082

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Abstract

Receptor-like protein tyrosine phosphatase κ (PTPRK) has been indicated as a putative tumour suppressor in primary central nervous system lymphomas and colorectal cancer. The present study investigated the expression of PTPRK in prostate cancer and the biological impact of PTPRK on prostate cancer cells. The expression of the PTPRK protein and transcript in prostate cancer was examined using IHC and PCR. Knockdown of PTPRK in prostate cancer cells was performed using a specific anti-PTPRK transgene. The impact of PTPRK knockdown on prostate cancer cells was evaluated using in vitro cell models and the apoptosis was analysed using flow cytometry. PTPRK expression was increased in prostate cancer tissues and knockdown of PTPRK in PC-3 cells suppressed the in vitro cell growth in which an increased apoptotic population was seen. Accompanied with the knockdown of PTPRK, increased expression of caspase-3, caspase-8 and p53, and a decreased ID1 expression were evident in the cells. Furthermore, an increased tyrosine phosphorylated c-Jun N-terminal kinase (JNK) was seen in the PTPRK knockdown cells. The effect on apoptosis was diminished by a JNK inhibitor. In conclusion, PTPRK knockdown resulted in increased apoptosis leading to the inhibition of in vitro growth of prostate cancer cells. PTPRK is a key factor in coordinating apoptosis via the regulation of MAPK pathways, in particular the JNK pathway in prostate cancer cells.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine
Subjects:	Q Science > QH Natural history > QH301 Biology R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer) R Medicine > RM Therapeutics. Pharmacology
Publisher:	Spandidos Publications
ISSN:	1019-6439
Last Modified:	25 Oct 2022 10:14
URI:	https://orca.cardiff.ac.uk/id/eprint/61487

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