PDLIM4是一种肌动蛋白结合蛋白，可抑制前列腺癌细胞的生长。
PDLIM4, an actin binding protein, suppresses prostate cancer cell growth.
作者信息
Vanaja Donkena Krishna, Grossmann Michael E, Cheville John C, Gazi Mozammel H, Gong Aiyu, Zhang Jin San, Ajtai Katalin, Burghardt Thomas P, Young Charles Y F
机构信息
Department of Urology, Mayo Clinic College of Medicine, Mayo Clinic, Rochester, MN 55905, USA.
出版信息
Cancer Invest. 2009 Mar;27(3):264-72. doi: 10.1080/07357900802406319.
Abstract
We investigated the molecular function of PDLIM4 in prostate cancer cells. PDLIM4 mRNA and protein-expression levels were reduced in LNCaP, LAPC4, DU145, CWR22, and PC3 prostate cancer cells. The re-expression of PDLIM4 in prostate cancer cells has significantly reduced the cell growth and clonogenicity with G1 phase of cell-cycle arrest. We have shown the direct interaction of PDLIM4 with F-actin. Restoration of PDLIM4 expression resulted in reduction of tumor growth in xenografts. These results suggest that PDLIM4 may function as a tumor suppressor, involved in the control of cell proliferation by associating with actin in prostate cancer cells.
摘要
我们研究了PDLIM4在前列腺癌细胞中的分子功能。在LNCaP、LAPC4、DU145、CWR22和PC3前列腺癌细胞中，PDLIM4 mRNA和蛋白表达水平降低。在前列腺癌细胞中重新表达PDLIM4可显著降低细胞生长和克隆形成能力，并使细胞周期停滞于G1期。我们已经证明PDLIM4与F-肌动蛋白直接相互作用。恢复PDLIM4表达可导致异种移植瘤生长减少。这些结果表明，PDLIM4可能作为一种肿瘤抑制因子，通过与前列腺癌细胞中的肌动蛋白结合参与细胞增殖的控制。
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