Objective: DEP domain containing 1 (DEPDC1), aberrantly upregulated in various tumors, has been shown to be involved in the occurrence and development of tumors. This study aims to investigate pathophysiological roles of DEPDC1 in colorectal cancer (CRC). Materials and Methods: Expression level of DEPDC1 and suppressor of zest 12 (SUZ12) in CRC tissues and cell lines were analyzed by quantitative real-time polymerase chain reaction and immunohistochemistry. Staining with 5-bromo-2-deoxyuridine staining and colony formation assays were conducted to evaluate cell proliferation. Transwell or wound healing assay to evaluate invasion or migration, respectively. The effect on epithelial-mesenchymal transition (EMT) of CRC was determined by Western blot. Results: DEPDC1 and SUZ12 were increased in CRC tissues and cell lines. Silence of DEPDC1 suppressed cell proliferation, migration, and invasion of CRC. Moreover, DEPDC1 knockdown suppressed EMT of CRC. Mechanistically, the authors demonstrated silencing DEPDC1 decreased protein expression of SUZ12 and led to a remarkable reduction of trimethylation on the lysine 27 residue of histone H3 (H3K27Me3). Inhibitory ability of DEPDC1 knockdown on CRC progression was reversed by overexpression of SUZ12. Conclusions: DEPDC1 promoted CRC progression through regulation of SUZ12-mediated H3K27Me3, illuminating a novel DEPDC1-SUZ12 molecular axis as regulator in CRC progression and suggesting potential implications in treatment of CRC.
Keywords: CRC; DEPDC1; H3K27Me3; SUZ12; progression.