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PIM‐1 gene RNA interference induces growth inhibition and apoptosis of prostate cancer cells and suppresses tumor progression in vivo
Author(s) -
Zhang Tong,
Zhang Xiaoguang,
Ding Kejia,
Yang Kuo,
Zhang Zhihong,
Xu Yong
Publication year - 2010
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.21524
Subject(s) - lipofectamine , apoptosis , cancer research , rna interference , gene silencing , cell growth , transfection , medicine , cell cycle , small interfering rna , prostate cancer , cell , in vivo , tumor progression , genetic enhancement , cancer , biology , cell culture , gene , rna , biochemistry , genetics , microbiology and biotechnology , vector (molecular biology) , recombinant dna
Abstract Background The goal of this study was to investigate the roles of PIM‐1 in prostate cancer (CaP) cell proliferation and apoptosis, and to assess the potential of PIM‐1 as a target for CaP therapy. Methods Using RNAi technology, we knocked down the expression of PIM‐1 in PC‐3 cell. After siRNA transfection, cell morphology, cell proliferation, cell cycle, and apoptosis rate were analyzed. PIM‐1 siRNA with Lipofectamine were injected into xenograft models to evaluate its therapeutic effect. Results PIM‐1 siRNA significantly inhibited PIM‐1 expression. In vitro, silencing of the PIM‐1 gene resulted in irregular cell morphology, decreased cell proliferation, inhibition of cell‐cycle progression, and induction of apoptosis. Compared with control groups, intratumoral injection of PIM‐1 siRNA with Lipofectamine in nude mice dramatically suppressed PC‐3 tumor progression. Conclusions PIM‐1 could play important roles in the progression of CaP and may be an interesting target for CaP therapy. J. Surg. Oncol. 2010; 101:513–519. © 2010 Wiley‐Liss, Inc.