Gelsolin negatively regulates the activity of tumor suppressor p53 through their physical interaction in hepatocarcinoma HepG2 cells
Gelsolin negatively regulates the activity of tumor suppressor p53 through their physical interaction in hepatocarcinoma HepG2 cells
复制标题
DOI：
10.1016/j.bbrc.2011.07.034
复制
发表时间：
2011-08-19
影响因子：
3.1
通讯作者：
Choi, Kyung-Hee
中科院分区：
文献类型：
--
作者：
An, Joo-Hee;Kim, Jung-Woong;Choi, Kyung-Hee
作为一种转录因子，P53调控多种细胞反应，包括细胞周期控制、细胞凋亡和分化。在这项研究中，我们已经证明了一种肌动蛋白调节蛋白，明胶蛋白(GSN)，可以与P53物理上相互作用。肝癌细胞中GSN的过表达抑制了P53的核定位。此外，我们证明了GSN负调控p21启动子驱动的报告构建体依赖于p53的转录活性。此外，在转导GSN的HepG2细胞中，P53介导的细胞凋亡受到抑制。综上所述，这些结果表明，GSN与P53结合，这种相互作用通过将P53锚定在细胞质中而抑制P53诱导的细胞凋亡。(C)2011 Elsevier Inc.保留所有权利。
As a transcription factor, p53 modulates several cellular responses including cell-cycle control, apoptosis, and differentiation. In this study, we have shown that an actin regulatory protein, gelsolin (GSN), can physically interact with p53. The nuclear localization of p53 is inhibited by GSN overexpression in hepatocarcinoma HepG2 cells. Additionally, we demonstrate that GSN negatively regulates p53-dependent transcriptional activity of a reporter construct, driven by the p21-promoter. Furthermore, p53-mediated apoptosis was repressed in GSN-transfected HepG2 cells. Taken together, these results suggest that GSN binds to p53 and this interaction leads to the inhibition of p53-induced apoptosis by anchoring of p53 in the cytoplasm in HepG2 cells. (C) 2011 Elsevier Inc. All rights reserved.