Study On Function And Molecular Mechanism Of SLC3A2 In The Proliferation Of Osteosarcoma

Growing evidences indicate that Solute carrier family 3 member 2(SLC3A2)is upregulated in multiple cancers and is related to tumor growth.We perform this study with the purpose to reveal the relationship between SLC3A2 and human osteosarcoma,and to uncover the biological role of SLC3A2 in osteosarcoma as well as the underlying biological mechanisms.Several experimental methods were used in this study.Western blot analysis,immunohistochemistry(IHC)and real time PCR were used to measure the SLC3A2 expression in human osteosarcoma samples as well as the human osteosarcoma cell lines.Cell counting kit 8(CCK-8),colony-forming assays and cell cycle assays were applied to measure the human osteosarcoma cell survival capacity and proliferation rate.Transwell assay was used with the purpose to measure capacity of cell migration and invasion.Besides,a slide based antibody array was used to investigate the potential molecular mechanism through which SLC3A2 regulates human osteosarcoma survival and growth.We found through this experiment that SLC3A2 was up-regulated in human osteosarcoma tissues as well as osteosarcoma cell lines.The high expression of SLC3A2 in osteosarcoma was correlated with tumor size and clinical stage of the tumor.Reduced expression of SLC3A2 in osteosarcoma cell inhibits its proliferation through cell cycle phase G2/M arrest.Most importantly,we found that the PI3K/Akt signaling pathway might be the potential way through which SLC3A2 regulates human osteosarcoma cells proliferation and growth.SLC3A2 is upregulated in human osteosarcoma and plays a crucial role in its growth.SLC3A2 may become a novel target for the treatment of human osteosarcoma.