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Effects of oleic acid on cell proliferation through an integrin-linked kinase signaling pathway in 786-O renal cell carcinoma cells

机译:油酸通过整合素连接激酶信号通路对786-O肾细胞癌细胞增殖的影响

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摘要

An increased risk of renal cell carcinoma (RCC) has been linked with obesity and metabolic syndrome. However, the mechanisms by which lipid metabolic disorders affect the development of RCC remain unclear and highly controversial. Integrin-linked kinase (ILK) is a serine/threonine protein kinase involved in the regulation of tumor cell growth and angiogenesis. In the present study, the effect of free fatty acids in the promotion of RCC progression was investigated by upregulating ILK. Results of the MTT assay indicated that treatment of 786-O cells with oleic acid induced a concentration-dependent increase in cell viability. Flow cytometry analysis revealed that the effect of oleic acid on cell apoptosis was not significant. Following treatment with oleic acid, the expression of ILK, phospho-Akt and G protein-coupled receptor 40 (GPR40) was increased in 786-O cells. These effects were reversed when the expression of ILK was downregulated using specific small interfering RNA. These results indicate that free fatty acids are associated with the development of renal cell carcinoma via activation of the GPR40/ILK/Akt pathway, revealing a novel mechanism for the correlation between metabolic disturbance and renal carcinoma.
机译:肥胖和代谢综合症与肾细胞癌(RCC)的风险增加有关。但是,脂质代谢紊乱影响RCC发生的机制仍然不清楚,并且存在很大争议。整联蛋白连接激酶(ILK)是一种丝氨酸/苏氨酸蛋白激酶,参与调节肿瘤细胞的生长和血管生成。在本研究中,通过上调ILK来研究游离脂肪酸在促进RCC进展中的作用。 MTT分析的结果表明,用油酸处理786-O细胞可诱导细胞存活率呈浓度依赖性增加。流式细胞仪分析表明,油酸对细胞凋亡的影响不明显。用油酸处理后,在786-O细胞中ILK,磷酸化Akt和G蛋白偶联受体40(GPR40)的表达增加。当使用特定的小分子干扰RNA下调ILK的表达时,这些作用将被逆转。这些结果表明,游离脂肪酸通过激活GPR40 / ILK / Akt途径与肾细胞癌的发展有关,揭示了代谢紊乱与肾癌之间相关性的新机制。

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