DNAJC2 is reversely regulated by miR‑627‑3p, promoting the proliferation of colorectal cancer

Liu,Hongfu; Li,Juan; Zhao,Huali; Liu,Xiaohui; Ye,Xinying

doi:10.3892/mmr.2021.12228

DNAJC2 is reversely regulated by miR‑627‑3p, promoting the proliferation of colorectal cancer

Authors:
- Hongfu Liu
- Juan Li
- Huali Zhao
- Xiaohui Liu
- Xinying Ye
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Affiliations: Department of General Surgery, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, P.R. China, Department of Dermatology and Venereal Diseases, Guiyang Center for Disease Control and Prevention, Guiyang, Guizhou 550000, P.R. China, Department of Pediatric, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, P.R. China, Department of Oncology, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, P.R. China
Published online on: June 16, 2021 https://doi.org/10.3892/mmr.2021.12228
Article Number: 589
Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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.

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