Objective To investigate the impact of DNA damage-regulated autophagy factor 2(DRAM2)on the proliferation and migration of non-small cell lung cancer(NSCLC)cells through tumor protein p53(p53)and autophagy.Methods DRAM2 gene was knocked down using lentiviral technology to establish NSCLC cell lines,and autophagy markers were detected by immunofluorescence and Western blot.CCK8 and Transwell assays were used to detect cell proliferation and migration.The effects of autophagy activation and p53 knockdown on autoph-agy and functions of DRAM2?knockdown cells were examined.Results Knockdown of DRAM2 inhibited NSCLC cells,with upregulation of p62 expression(P<0.05)and decreased level of LC3?Ⅱ(P<0.05).Knockdown of DRAM2 suppressed the proliferation(P<0.001)and migration(P<0.001)of NSCLC cells.Activation of auto?phagy partially reversed the inhibitory effects of DRAM2 knockdown on cell proliferation(P<0.01)and migration(P<0.01).When DRAM2 and p53 were knocked down simultaneously,autophagy,cell proliferation(P<0.05)and migration abilities(P<0.001)were restored.Conclusions Knockdown of DRAM2 inhibits the proliferation and migration of lung cancer cell line A549,providing a potential intervention direction for the devel?opment of therapeutic strategies.

Objective To investigate the impact of DNA damage-regulated autophagy factor 2(DRAM2)on the proliferation and migration of non-small cell lung cancer(NSCLC)cells through tumor protein p53(p53)and autophagy.Methods DRAM2 gene was knocked down using lentiviral technology to establish NSCLC cell lines,and autophagy markers were detected by immunofluorescence and Western blot.CCK8 and Transwell assays were used to detect cell proliferation and migration.The effects of autophagy activation and p53 knockdown on autoph-agy and functions of DRAM2?knockdown cells were examined.Results Knockdown of DRAM2 inhibited NSCLC cells,with upregulation of p62 expression(P<0.05)and decreased level of LC3?Ⅱ(P<0.05).Knockdown of DRAM2 suppressed the proliferation(P<0.001)and migration(P<0.001)of NSCLC cells.Activation of auto?phagy partially reversed the inhibitory effects of DRAM2 knockdown on cell proliferation(P<0.01)and migration(P<0.01).When DRAM2 and p53 were knocked down simultaneously,autophagy,cell proliferation(P<0.05)and migration abilities(P<0.001)were restored.Conclusions Knockdown of DRAM2 inhibits the proliferation and migration of lung cancer cell line A549,providing a potential intervention direction for the devel?opment of therapeutic strategies.

Objective This study aimed to explore the expression pattern of transmembrane protein 33(TMEM33)in lung adenocarcinoma and its correlation with clinical pathological features.Methods Bioinformatics tools and public databases(e.g.,TCGA and GEO)were used to analyze TMEM33 expression data in lung cancer.Then,immunoblotting and real-time quantitative PCR were performed to detect TMEM33 protein and mRNA levels in four cell lines.Immunofluorescence and immunohistochemistry were also used to assess TMEM33 expression and localization in lung adenocarcinoma and normal lung tissue samples.Results Bioinformatics analysis revealed higher TMEM33 expression in lung adenocarcinoma than in normal lung tissue(P＜0.05)and a significant correlation between TMEM33 and SLC30A9 expression(P＜0.0001).Logistic regression analysis indicated an association between TMEM33 expression and tumor T stage(OR=0.48,P=0.044).Experimental results showed higher TMEM33 protein(P＜0.01)and mRNA(P＜0.001)levels in lung adenocarcinoma cell lines than in normal lung epithelial cells.Similarly,TMEM33 protein(P＜0.05)and mRNA(P＜0.01)levels were higher in lung adenocarcinoma tissues than in adjacent tissues.Immunohistochemistry confirmed high TMEM33 expression in lung adenocarcinoma tissues.Conclusion TMEM33 is highly expressed in lung adenocarcinoma,associated with malignancy and T stage,and may be a potential prognostic and therapeutic target.

Transmembrane protein 33(TMEM33)is up-regulated in the majority of cancers.To change the expression of TMEM33 can significantly affect the proliferation,migration,and invasion of renal and cervical cancer cells.Its mechanisms of action may involve four aspects:1)participation in lipid metabolism;2)regu-lation of endoplasmic reticulum;3)regulation of intracellular calcium homeostasis;4)participation in angio-genesis.