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瘦素可上调 MCF-7 乳腺癌细胞端粒酶活性和人端粒酶逆转录酶的转录。

Leptin upregulates telomerase activity and transcription of human telomerase reverse transcriptase in MCF-7 breast cancer cells.

机构信息

Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Tianjin Medical University Cancer Hospital, Tianjin, China.

出版信息

Biochem Biophys Res Commun. 2010 Mar 26;394(1):59-63. doi: 10.1016/j.bbrc.2010.02.093. Epub 2010 Feb 18.

Abstract

The aim was to analyze the mechanism of leptin-induced activity of telomerase in MCF-7 breast cancer cells. We found that leptin activated telomerase in a dose-dependent manner; leptin upregulated the expression of Human Telomerase Reverse Transcriptase (hTERT) at mRNA and protein levels; blockade of signal transducer and activator of transcription 3 (STAT3) phosphorylation significantly counteracted leptin-induced hTERT transcription and protein expression; chromatin immunoprecipitation analysis showed that leptin enhanced the binding of STAT3 to the hTERT promoter. This study uncovers a new mechanism of the proliferative effect of leptin on breast cancer cells and provides a new explanation of obesity-related breast cancer.

摘要

目的在于分析瘦素诱导 MCF-7 乳腺癌细胞端粒酶活性的机制。我们发现瘦素呈剂量依赖性地激活端粒酶;瘦素上调 hTERT 在 mRNA 和蛋白水平的表达;信号转导和转录激活因子 3(STAT3)磷酸化阻断明显拮抗瘦素诱导的 hTERT 转录和蛋白表达;染色质免疫沉淀分析表明,瘦素增强了 STAT3 与 hTERT 启动子的结合。本研究揭示了瘦素对乳腺癌细胞增殖作用的新机制,并为肥胖相关乳腺癌提供了新的解释。

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