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毒蕈碱型乙酰胆碱受体促进SNU - 407人结肠癌细胞的增殖

Enhanced proliferation of SNU-407 human colon cancer cells by muscarinic acetylcholine receptors.

作者信息

Park Yang-Seo, Cho Nam Jeong

机构信息

School of Life Sciences, Chungbuk National University, Cheongju, Korea.

出版信息

BMB Rep. 2008 Nov 30;41(11):803-7. doi: 10.5483/bmbrep.2008.41.11.803.

Abstract

We investigated the expression of muscarinic acetylcholine receptors (mAChRs) and their possible involvement in the regulation of cell proliferation in four colon cancer cell lines (SNU-61, SNU-81, SNU-407, and SNU-1033) derived from Korean colon carcinoma patients. A ligand binding assay showed that all four cell lines expressed mAChRs. Treatment of the four cell lines with the cholinergic agonist carbachol led to the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2). In SNU-407 cells, carbachol significantly stimulated cell proliferation, which could be abolished by the muscarinic antagonist atropine and the ERK1/2 kinase inhibitor PD98059. These results indicate that mAChRs specifically mediate the proliferation of SNU-407 colon cancer cells via the ERK1/2 pathway.

摘要

我们研究了毒蕈碱型乙酰胆碱受体(mAChRs)的表达及其在源自韩国结肠癌患者的四种结肠癌细胞系(SNU - 61、SNU - 81、SNU - 407和SNU - 1033)细胞增殖调控中的可能作用。配体结合试验表明,所有四种细胞系均表达mAChRs。用胆碱能激动剂卡巴胆碱处理这四种细胞系导致细胞外信号调节激酶1和2(ERK1/2)激活。在SNU - 407细胞中,卡巴胆碱显著刺激细胞增殖,这可被毒蕈碱拮抗剂阿托品和ERK1/2激酶抑制剂PD98059消除。这些结果表明,mAChRs通过ERK1/2途径特异性介导SNU - 407结肠癌细胞的增殖。

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