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Silencing Of PRR11 Suppresses Cell Proliferation And Induces Autophagy In NSCLC Cells

Posted on:2019-05-28Degree:MasterType:Thesis
Country:ChinaCandidate:L ZhangFull Text:PDF
GTID:2394330566482149Subject:Biochemistry and Molecular Biology
Abstract/Summary:PDF Full Text Request
Our previous studies have demonstrated that proline-rich protein 11(PRR11)is a novel tumor-related gene and implicates in regulating the proliferation in lung cancer.However,its precise role in cell cycle progression remains unclear.Our recent evidences show PRR11 have an effect on autophagy in non-small-cell lung cancer(NSCLC)cells.Two human NSCLC cell lines H1299 and A549 are transiently transfected with against PRR11 si RNA.The Cell Counting Kit-8 and plate clone formation assay show that downregulation of PRR11 inhibits the cell proliferation.And our data suggest that PRR11 depletion enhances the autophagosomes formation,followed with downregulation of P62 and upregulation of LC3-II protein.Furthermore,the immunoblotting results indicates that PRR11 depletion inactivates the Akt/mTOR signaling pathway.Collectively,these results demonstrate PRR11 has an effective role in autophagy in NSCLC cells through Akt/mTOR autophagy signaling pathways.Therefore,it is helpful to clarify the function of PRR11 in tumorigenesis of NSCLC.
Keywords/Search Tags:Akt/mTOR, autophagy, cell proliferation, non-small-cell lung cancer, PRR11
PDF Full Text Request
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