首页> 美国卫生研究院文献>International Journal of Clinical and Experimental Pathology >Prostaglandin transporter SLCO2A1 mediates the invasion and apoptosis of lung cancer cells via PI3K/AKT/mTOR pathway
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Prostaglandin transporter SLCO2A1 mediates the invasion and apoptosis of lung cancer cells via PI3K/AKT/mTOR pathway

机译:前列腺素转运蛋白SLCO2A1通过PI3K / AKT / mTOR途径介导肺癌细胞的侵袭和凋亡

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摘要

Treatment of lung cancer involves regulation of various key factors in many signaling pathways. The prostaglandin transporter, solute carrier organic anion transporter family member 2A1 (SLCO2A1), is a promising regulatory factor of cancer cells. By analyzing the invasion and apoptosis status of lung cancer cells, and detecting the expression changes of key factors in PI3K/AKT/mTOR pathway after overexpression and knockdown of SLCO2A1 in vitro, this study intended to investigate the function of SLCO2A1 in mediating lung cancer cells. Results showed overexpression of SLCO2A1 could induce the invasion of lung cancer cells, and its knockdown inhibited the invasion and induced the apoptosis of cells. mTOR, AKT and S6 in PI3K/AKT/mTOR pathway were not affected by SLCO2A1. But the expression levels of p-mTOR, p-AKT and p-S6 were up-regulated or down-regulated with the overexpression or knockdown of SLCO2A1. Thus SLCO2A1 was inferred to mediate the invasion and apoptosis of lung cancer cells via PI3K/AKT/mTOR pathway. These results implied SLCO2A1 could be a regulatory factor of the invasion and apoptosis of lung cancer cells and serve as a promising target for lung cancer therapy.
机译:肺癌的治疗涉及许多信号通路中各种关键因素的调节。前列腺素转运蛋白,溶质载体有机阴离子转运蛋白家族成员2A1(SLCO2A1),是癌细胞的有希望的调节因子。通过分析SLCO2A1在体外的过度表达和敲低后肺癌细胞的侵袭和凋亡状态,并检测PI3K / AKT / mTOR途径中关键因子的表达变化,旨在研究SLCO2A1在介导肺癌细胞中的功能。 。结果表明,SLCO2A1过表达可诱导肺癌细胞侵袭,其敲低抑制其侵袭并诱导细胞凋亡。 PICO3 / AKT / mTOR途径中的mTOR,AKT和S6不受SLCO2A1的影响。但是随着SLCO2A1的过表达或敲低,p-mTOR,p-AKT和p-S6的表达​​水平被上调或下调。因此推断SLCO2A1通过PI3K / AKT / mTOR途径介导肺癌细胞的侵袭和凋亡。这些结果暗示SLCO2A1可能是肺癌细胞侵袭和凋亡的调控因子,并有望成为肺癌治疗的靶标。

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