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Inhibition of proliferation of human lung cancer cells by green tea catechins is mediated by upregulation of let-7

机译:绿茶儿茶素对人肺癌细胞增殖的抑制作用由let-7的上调介导

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摘要

Green tea catechins are known to function as anticancer agents via inhibition of carcinogenesis during the initiation, promotion and progression stages. Many potential mechanisms have been proposed, yet the precise mechanism of lung cancer prevention by green tea catechins remains unclear. microRNAs (miRs) are a class of 21–24 nucleotide small non-coding RNAs and play critical roles throughout cellular development and regulation. Emerging evidence demonstrates that tea catechins influence the expression of miRs in human cancer cells to inhibit tumorigenesis. Both let-7a-1 and let-7g were detected in the human lung cancer cells treated with tea catechins. The cell viability and cell cycle were analyzed after tea catechins treatment. In the present study, we found that tea catechins upregulated the tumor-suppressor miRs, let-7a-1 and let-7g, in lung cancer cell lines. The upregulation of let-7a/7g repressed the expression of their targets, C-MYC and the regulatory protein of LIN-28, at the mRNA and protein levels. Moreover, the cell growth assay indicated that tea catechins significantly inhibited cell proliferation, and the flow cytometric analysis revealed an increase in the number of cells in the G2/M phase and a decrease in the number of cells in the S phase after treatment with tea catechins. These observations suggest that green tea catechins mediate the inhibition of proliferation of lung cancer cells through the let-7 signaling pathway.
机译:已知绿茶儿茶素通过在起始,促进和发展阶段抑制癌变而起抗癌剂的作用。已经提出了许多潜在的机制,但是尚不清楚绿茶儿茶素预防肺癌的确切机制。 microRNA(miRs)是一类21–24核苷酸的小型非编码RNA,在整个细胞发育和调控过程中都起着至关重要的作用。新兴证据表明,茶儿茶素会影响人类癌细胞中miRs的表达,从而抑制肿瘤发生。在用茶儿茶素处理的人肺癌细胞中检测到let-7a-1和let-7g。茶儿茶素处理后分析细胞活力和细胞周期。在本研究中,我们发现茶儿茶素上调肺癌细胞系中的肿瘤抑制物miRs let-7a-1和let-7g。 let-7a / 7g的上调抑制了其靶标C-MYC和LIN-28调控蛋白在mRNA和蛋白水平上的表达。此外,细胞生长测定表明茶儿茶素显着抑制细胞增殖,流式细胞仪分析显示,用茶处理后,G2 / M期的细胞数量增加而S期的细胞数量减少。儿茶素。这些观察结果表明,绿茶儿茶素通过let-7信号通路介导了肺癌细胞增殖的抑制作用。

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