Abstract
It has been reported that DEP domain protein 1B (DEPDC1B) serves several roles in the occurrence and development of various types of cancer. Nevertheless, the effect of DEPDC1B on colorectal cancer (CRC), as well as its particular underlying molecular mechanism remain to be elucidated. In the present study, the mRNA and protein expression levels of DEPDC1B and nucleoporin 37 (NUP37) in CRC cell lines were assessed by reverse transcription‑quantitative PCR and western blotting, respectively. Cell Counting Kit‑8 and 5‑Ethynyl‑2'‑deoxyuridine assays were carried out to determine cell proliferation. In addition, the migration and invasion abilities of cells were evaluated using wound healing and Transwell assays. The changes in cell apoptosis and cell cycle distribution were assessed by flow cytometry and western blotting. Bioinformatics analysis and co‑immunoprecipitation assays were performed to predict and verify, respectively, the binding capacity of DEPDC1B on NUP37. The expression levels of Ki‑67 were detected by immunohistochemical assay. Finally, the activation of phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling was measured using western blotting. The results showed that DEPDC1B and NUP37 were upregulated in CRC cell lines. DEPDC1B and NUP37 silencing both inhibited the proliferation, migration and invasion capabilities of CRC cells and promoted cell apoptosis and cell cycle arrest. Furthermore, NUP37 overexpression reversed the inhibitory effects of DEPDC1B silencing on the behavior of CRC cells. Animal experiments demonstrated that DEPDC1B knockdown inhibited the growth of CRC in vivo by targeting NUP37. In addition, DEPDC1B knockdown inhibited the expression levels of the PI3K/AKT signaling‑related proteins in CRC cells and tissues by also binding to NUP37. Overall, the current study suggested that DEPDC1B silencing could alleviate the progression of CRC via targeting NUP37.