The Role Of Oncoprotein DEPDC1 And The Underlying Mechanisms In A549 Lung Cancer Cells

Objective:Ectopic expression of DEP domain containing protein 1(DEPDC1)in lung adenocarcinomas is associated with poor prognosis,but its role and the underlying mechanism remain unknown.In this study,the role of DEPDC1 in lung cancer A549 cells was investigated.Methods:We examined DEPDC1 expression in lung cancer cell lines with Western blot assay and DEPDC1-postitive cell A549 was selected for further experiments.MicroRNA-130a(miR-130a)was expressed to detect whether and how DEPDC1 regulates the proliferation in A549 cell.The optimal concentration of 11R-DEP:611-628 peptide was screened with CCK-8 assay,then we treated A549 cell with 5 μM peptide and explored the anti-apoptosis mechanism of DEPDC1 by immunofluorescence staining and flow cytometry assay.Then,JNK inhibitor was used to treat A549 cells,and we detected the role of JNK in A549.Results: Our results indicate that DEPDC1 was highly expressed in lung cancer cells.We found that miR-130 a and 11R-DEP:611-628 peptide(5 μM)both inhibited A549 proliferation and induced apoptosis.We observed that 11R-DEP:611-628 peptide treatment resulted in elevated A20 expression,dramatically reduced nuclear NF-κB and increased phosphor-JNK.These findings indicate that DEPDC1 inhibits apoptosis of A549 cell via suppressing A20 expression to regulate NF-κB activity,and that JNK plays a protective role upon 11R-DEP:611-628 peptide treatment.Conclusions: 1.MiR-130 a and 11R-DEP:611-628 peptide both inhibit A549 proliferation and induce apoptosis;2.DEPDC1 inhibits apoptosis of A549 cell via suppressing A20 expression to regulate NF-κB activity;3.11R-DEP:611-628 peptide induces A549 apoptosis,which can be inhibited by increasing JNK activity.