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miR‐663 Induces Castration‐Resistant Prostate Cancer Transformation and Predicts Clinical Recurrence
Author(s) -
Jiao Li,
Deng Zhen,
Xu Chuanliang,
Yu Yongwei,
Li Yun,
Yang Chun,
Chen Junyi,
liu Zhiyong,
Huang Gang,
Li LongCheng,
Sun Yinghao
Publication year - 2014
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.24510
Subject(s) - prostate cancer , lncap , downregulation and upregulation , medicine , oncomir , cancer research , prostate , oncology , stage (stratigraphy) , biochemical recurrence , cancer , carcinogenesis , prostatectomy , biology , gene , biochemistry , paleontology
Castration‐resistant prostate cancer (CRPC) and its treatment are challenging issues in prostate cancer management. Here, we report that miR‐663 is upregulated in CRPC tissues. Overexpression of miR‐663 in prostate LNCaP cells promotes cell proliferation and invasion, neuroendocrine differentiation, and reduction in dihydrotestosterone‐induced upregulation of prostate‐specific antigen expression. Furthermore, results of in situ hybridization show that miR‐663 expression is correlated with Gleason score and TNM stage and is an independent prognostic predictor of clinical recurrence. Together, these findings suggest that miR‐663 is a potential oncomiR for CRPC and may serve as a tumor biomarker for the early diagnosis of CRPC. J. Cell. Physiol. 229: 834–844, 2014. © 2013 Wiley Periodicals, Inc.

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