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Li Yi,Peng Feng,Tan Xiangyun,Wang Jin,Xu Yeqing 한국유전학회 2021 Genes & Genomics Vol.43 No.10
Background Colorectal cancer (CRC) exhibits high risks of morbidity and mortality. Objective To investigate the efect of scavenger receptor class A member 5 (SCRAR5) on CRC and its mechanism on modulation of cancer development. Methods The SCRAR5 expression in four kinds of CRC cell lines (SW620, SW480, HT29, and HCT116) was measured by quantitative PCR and western blotting, respectively. The efects of SCRAR5 abnormal expression on cell proliferation, apoptosis, and migration were analyzed by CCK-8 assay, EdU assay, colony-forming assay, fow cytometry assay, Transwell assay and wound healing assay, respectively. Meanwhile, the involvements of PI3K/AKT/mTOR pathway with the role of SCRAR5 were investigated by western blotting. Afterwards, the in vivo efects of SCRAR5 abnormal expression on CRC xenograft mice were fnally investigated by evaluating tumor volume, apoptosis and Ki67 expression. Results SCRAR5 was lowly expressed in CRC cell lines, especially SW480 cells. Up-regulation of SCRAR5 signifcantly promoted cell apoptosis, reduced cell proliferation and migration in SW480 cells. Notably, SCRAR5 overexpression obviously inhibited the phosphorylation levels of PI3K, AKT, and mTOR. Reversely, SCRAR5 silence exhibited promoting efects on HT29 cells. Consistently, in vivo experiments also revealed that SCRAR5 overexpression remarkably suppressed tumor volume and Ki67 expression, as well as promoted cell apoptosis. Conclusions Overall, up-regulating of SCRAR5 obviously inhibited CRC tumor growth in vitro and in vivo, which might be related to PI3K/AKT/mTOR pathway.
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