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suck abstract from ncbi


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pmid26464663
      Int+J+Clin+Exp+Pathol 2015 ; 8 (8 ): 9175-81
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  • Prostaglandin transporter, SLCO2A1, mediates the invasion and apoptosis of lung cancer cells via PI3K/AKT/mTOR pathway #MMPMID26464663
  • Zhu Q ; Liang X ; Dai J ; Guan X
  • Int J Clin Exp Pathol 2015[]; 8 (8 ): 9175-81 PMID26464663 show ga
  • 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.
  • |Apoptosis/*genetics [MESH]
  • |Carcinoma, Non-Small-Cell Lung/*genetics/metabolism/pathology [MESH]
  • |Cell Line, Tumor [MESH]
  • |Cell Proliferation/genetics [MESH]
  • |Down-Regulation [MESH]
  • |Humans [MESH]
  • |Lung Neoplasms/*genetics/metabolism/pathology [MESH]
  • |Neoplasm Invasiveness/*genetics/pathology [MESH]
  • |Organic Anion Transporters/*genetics/metabolism [MESH]
  • |Phosphatidylinositol 3-Kinases/metabolism [MESH]
  • |Phosphorylation [MESH]
  • |Proto-Oncogene Proteins c-akt/metabolism [MESH]
  • |Signal Transduction/*genetics [MESH]
  • |TOR Serine-Threonine Kinases/metabolism [MESH]


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