Zhu Qiaoliang, Liang Xiang, Dai Jing, Guan Xin
Department of Thoracic Surgery Shanghai 9th People's Hospital Shanghai 200011, China.
Department of Cadres Health Care, Third Hospital of Shijiazhuang Shijiazhuang 050011, China.
Int J Clin Exp Pathol. 2015 Aug 1;8(8):9175-81. eCollection 2015.
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.
肺癌的治疗涉及多种信号通路中各种关键因子的调控。前列腺素转运体，溶质载体有机阴离子转运体家族成员2A1（SLCO2A1），是一种很有前景的癌细胞调节因子。通过分析肺癌细胞的侵袭和凋亡状态，并在体外过表达和敲低SLCO2A1后检测PI3K/AKT/mTOR通路中关键因子的表达变化，本研究旨在探讨SLCO2A1在介导肺癌细胞中的功能。结果显示，SLCO2A1的过表达可诱导肺癌细胞的侵袭，而其敲低则抑制细胞侵袭并诱导细胞凋亡。PI3K/AKT/mTOR通路中的mTOR、AKT和S6不受SLCO2A1影响。但随着SLCO2A1的过表达或敲低，p-mTOR、p-AKT和p-S6的表达水平上调或下调。因此推断SLCO2A1通过PI3K/AKT/mTOR通路介导肺癌细胞的侵袭和凋亡。这些结果表明SLCO2A1可能是肺癌细胞侵袭和凋亡的调节因子，有望成为肺癌治疗的靶点。
