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热休克因子1调节人宫颈癌细胞系中hsa-miR-432的表达。

Heat shock factor 1 regulates hsa-miR-432 expression in human cervical cancer cell line.

作者信息

Das Srijit, Bhattacharyya Nitai Pada

机构信息

Crystallography & Molecular Biology Division, Saha Institute of Nuclear Physics, 1/AF Bidhannagar, Kolkata 700064, India.

Crystallography & Molecular Biology Division, Saha Institute of Nuclear Physics, 1/AF Bidhannagar, Kolkata 700064, India; Biomedical Genomics Centre, PG Polyclinic Building, 5, Suburbun Hospital Road, Kolkata 700020, India.

出版信息

Biochem Biophys Res Commun. 2014 Oct 24;453(3):461-6. doi: 10.1016/j.bbrc.2014.09.100. Epub 2014 Oct 1.

Abstract

Heat shock response pathway is a conserved defense mechanism of mammalian cells to maintain protein homeostasis against proteotoxic environmental conditions. This is characterized by robust synthesis of molecular chaperones mostly by stress-induced activation of heat shock factor 1 (HSF1). MicroRNAs (miRNAs) are a family of small non-coding RNAs that negatively regulate expression of protein-coding genes. Here we report altered expression of a set of miRNAs by thermal stress in HeLa cells. We also show that HSF1 regulates hsa-miR-432 expression in heat shock-dependent manner through its cognate binding site present in hsa-miR-432 upstream sequence. Our report uncovers a novel function of HSF1 and indicates involvement of miRNAs in HSF1-mediated protection of cellular proteome.

摘要

热休克反应途径是哺乳动物细胞在蛋白毒性环境条件下维持蛋白质稳态的一种保守防御机制。其特征是主要通过应激诱导热休克因子1(HSF1)的激活来大量合成分子伴侣。微小RNA(miRNA)是一类小的非编码RNA,可负向调节蛋白质编码基因的表达。在此,我们报告了热应激导致HeLa细胞中一组miRNA的表达发生改变。我们还表明,HSF1通过其在hsa-miR-432上游序列中的同源结合位点以热休克依赖的方式调节hsa-miR-432的表达。我们的报告揭示了HSF1的一种新功能,并表明miRNA参与了HSF1介导的细胞蛋白质组保护。

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