National Centre for Cell Science, Pune University Campus, Ganeshkhind, Pune, India.
FEBS Lett. 2010 Mar 19;584(6):1187-92. doi: 10.1016/j.febslet.2010.02.025. Epub 2010 Feb 11.
Here, we report Prostaglandin A2 (PGA2) induced binding of HSP70 to a novel site on phi1 SMAR1 5' UTR which stabilizes the wild type transcript and leads to subsequent increase in SMAR1 protein levels. SMAR1 mediated cell cycle arrest is perturbed in PGA2-treated cells when HSP70 is knocked-down. Contrarily HSP70, unlike SMAR1, is overexpressed in breast cancers. We demonstrate that this is because of the inability of HSP70 to bind to the phi17 SMAR1 UTR variant which is the predominant form in breast cancers.
在这里，我们报告前列腺素 A2 (PGA2) 诱导 HSP70 与 phi1 SMAR1 5'UTR 上的一个新位点结合，该位点稳定野生型转录本，并导致随后 SMAR1 蛋白水平的增加。在 HSP70 敲低的 PGA2 处理细胞中，SMAR1 介导的细胞周期停滞受到干扰。相反，HSP70 不像 SMAR1 那样在乳腺癌中过表达。我们证明这是因为 HSP70 无法与在乳腺癌中占主导形式的 phi17 SMAR1 UTR 变体结合。
