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Expert Opin Ther Targets. 2017 Sep;21(9):911-920. doi: 10.1080/14728222.2017.1369044. Epub 2017 Aug 23.

Implications of Bcl-2 and its interplay with other molecules and signaling pathways in prostate cancer progression.

Author information

1
a Cancer Molecular Targeted Herbal Research Center, College of Korean Medicine , Kyung Hee University , Seoul , South Korea.
2
b Department of East West Medical Science, Graduate School of East West Medical Science , Kyung Hee University , Yongin , South Korea.

Abstract

Among several genetic alterations involved in the progression of prostate cancer, B cell lymphoma gene number 2 (BCL-2) is an important target molecule in the progression of androgen-independent prostate cancer (AIPC) after androgen ablation or castration. Nevertheless, the molecular mechanism of BCL-2 in prostate cancer progression remains elusive and controversial. In the current review, we discuss the critical role of BCL-2 in the carcinogenesis of prostate cancer with experimental evidences on the BCL-2 molecular networks in AIPC and androgen-dependent prostate cancer (ADPC) and subsequently suggest perspective research targeting BCL-2. Areas covered: This review focused on the molecular implications of BCL-2 in association with other molecules and signaling pathways involved in the progression and carcinogenesis of prostate cancer. Expert opinion: BCL-2 plays a pivotal role in the progression of AIPC than in ADPC since androgen represses BCL-2. BCL-2 acts as a pro-survival molecule in association with androgen-related signaling in the progression of ADPC, while BCL-2 upregulation, PTEN loss, PI3K/AKT phosphorylation and receptor tyrosine kinase (RTK) activation are primarily involved in AIPC. To identify more effective prostate cancer therapy, further mechanistic studies are required with BCL-2 inhibitors in AIPC and ADPC, considering a multi-target therapy against BCL-2 and its related signaling.

KEYWORDS:

AKT; BCL-2; PTEN; androgen; microRNAs; prostate cancer

PMID:
28816549
DOI:
10.1080/14728222.2017.1369044
[Indexed for MEDLINE]

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