hsa-miR-15a-5p inhibits colon cell carcinoma via targeting CCND1

Colon carcinoma is one of the most common cancers worldwide. Epidemiological studies have revealed that colon cancer is the third leading cause of cancer-related deaths, which is due to the increased incidence and mortality rates. However, the treatment strategies for colon cancer remain unsatisfactory for patients, especially for those with advanced or recurrent colon cancer. Dysregulated microRNAs (miRNAs) are considered to influence tumor development and metastasis. However, the molecular mechanism through which miRNAs affect cancer progression is not yet completely understood. The aim of the present study was to investigate the expression levels of has-miR-15a-5p and its molecular mechanism in colon cell carcinoma. In the present study, the expression levels of hsa-miR-15a-5p were found to be decreased in colon tumor tissues and cancer cell lines. Hsa-miR-15a-5p overexpression inhibited colon cell proliferation and migration. Mechanistically, the G1/S-specific cyclin-D1 (CCND1) gene was predicted as a target of hsa-miR-15a-5p, as evidenced by bioinformatics and dual-luciferase reporter assay analyses. CCND1 overexpression significantly increased the progression of colon cancer. Furthermore, CCND1 was demonstrated to mediate the effects of hsa-miR-15a-5p on colon cancer cells. The present study demonstrated that hsa-miR-15a-5p alleviated the proliferation, migration and invasion of colon cancer by targeting the CCND1 gene, which represents a potential molecular target for the diagnosis and treatment of colon cancer.

Automated summary

Colon carcinoma is a common cancer with unsatisfactory treatment strategies, especially for advanced cases. Dysregulated miRNAs are believed to impact tumor development, with has-miR-15a-5p found to inhibit proliferation and migration of colon cancer cells by targeting the CCND1 gene. This study suggests that has-miR-15a-5p could serve as a potential molecular target for the diagnosis and treatment of colon cancer.