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发表于 2015-10-8 00:41
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来自:江苏
作者论述毫无逻辑可言,缺乏研究依据
8 ~' V) ]. G6 _9 \我随便搜了一下就已经找到 1999年发表在Oncogene 上的一篇关于酸性环境诱发细胞自我凋亡的临床研究3 f) W7 m" _! R% t; J
http://www.nature.com/onc/journal/v18/n21/full/1202660a.html4 m; ]' v% [6 v' Q
An acidic environment leads to p53 dependent induction of apoptosis in human adenoma and carcinoma cell lines: implications for clonal selection during colorectal carcinogenesis+ p1 o- N7 i( }5 t% q+ ?
A C Williamsa, T J Collard and C Paraskeva8 a: O! M! A& H
CRC Colorectal Tumour Biology Research Group, Department of Pathology and Microbiology, School of Medical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK
. e r) L# U' [& G& u6 g5 S/ aAbstract6 r; r2 Y0 [8 g, r* _# P% A
As tumours are known to acidify their microenvironment and fluctuations in lumenal pH have been reported in a number of colonic disease conditions, we investigated whether loss of p53 function, commonly associated with the adenoma to carcinoma transition in human colorectal epithelium, was implicated in the cellular response to changes in extracellular pH. Human colonic adenoma and carcinoma derived cell lines were incubated at an inital pH range of 5.5 - 8.0 and the attached cell yield and apoptotic cell yield determined after 4 days. Exposure of all cell lines to an acidic growth environment was associated with a G1 arrest, down regulation of the retinoblastoma protein (pRb) protein and switch to the hypophosphorylated form of the protein, and increased expression of the p21 protein. However, induction of apoptosis, associated with increased p53 protein expression but not with changes in Bcl-2 expression, was only detected in the adenoma derived BH/C1 and AA/C1 cell lines which express wild type p53 activity. Furthermore, this induction of apoptosis was inhibited in the transfected cell line AA/273p53/B, in which the wild type p53 function has been abrogated. These results suggest that acidification of the microenvironment would provide a selective growth advantage for cells that have lost wild type p53 function, leading to clonal expansion of aberrant cell populations. |
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