Colorectal cancer (CRC) is one of the most common malignancies among human, which is often connected with increased incidence and mortality rate. DnaJ Heat Shock Protein Family (Hsp40) Member C2 (DNAJC2) is an epigenetic factor, which is involved in a number of cytological functions, such as transcriptional regulation and ubiquitination. A number of studies reveal that DNAJC2 is closely associated with several tumors. However, the function and mechanism of DNAJC2 in CRC remains to be elucidated. In the present study, the expression of DNAJC2 was detected in CRC tissues and adjacent normal tissues. The results indicated that DNAJC2 was increased in CRC tissues and the expression level of DNAJC2 was significantly associated with tumor size. Cell function was detected via Cell Counting Kit‑8, 5‑ethynyl‑2'‑deoxyuridine, colony formation assays and flow cytometry by upregulating or knocking down of DNAJC2. Overexpression of DNAJC2 could accelerate cell proliferation while suppression of DNAJC2 decreased cell proliferation, possibly via the regulation of cell cycle regulation in vitro. It was also found that the function of DNAJC2 was reversely regulated by miR‑672‑3p, causing the promoting of cell proliferation through the activation of AKT/P21 signal pathway in CRC cells. These results suggested that DNAJC2 is a tumor‑regulated protein in the progression of CRC and may represent a novel target for CRC detection and therapy.
Keywords: AKT; DnaJ Heat Shock Protein Family (Hsp40) Member C2; cell proliferation; colorectal cancer; microRNA.