Overexpression of DEPDC1B contributes to malignant progression and immune infiltration in lung adenocarcinoma
Dysregulated expression of DEPDC1B (DEP domain-containing protein 1B) has been reported to be implicated in various types of malignancies. However, its functional implication as well as the underlying molecular mechanism in lung adenocarcinoma (LUAD) remains elusive. In this study, the role and clinical significance of DEPDC1B in LUAD has been systematically investigated. Our results first showed that DEPDC1B is significantly upregulated in various types of cancers including LUAD, and high DEPDC1B expression is remarkably associated with poor survival in LUAD patients. Functional study demonstrated that DEPDC1B knockdown inhibited cell growth, cell cycle progression, colony formation, cell migration and motility. Furthermore, xenograft nude mouse model experiments showed that DEPDC1B silencing resulted in significant inhibition of tumor growth in vivo. Detailed mechanistic experiments revealed that DEPDC1B knockdown caused down-regulation of various downstream genes including NID1, FN1 and EGFR, and inactivation of multiple critical pathways including ERK and PI3K-AKT pathways. Overall design: To explore the  function of DEPDC1B in LUAD, we established A549 cell lines in which DEPDC1B gene has been knocked down by shRNA. And then total RNA were harvested, followed by cDNA library construction, and subjected to RNA-seq analysis.