MiR-17-5p Targets and Downregulates CADM2, Activating the Malignant Phenotypes of Colon Cancer Cells

• Published in: Molecular biotechnology 2022-12, Vol.64 (12), p.1388-1400
• Main Authors: Wang, Yang, Zhao, Jinlai, Wang, Yigang, Gao, Jianchao, Yang, Haichao, Li, Hua
• Format: Article
• Language: English
• Subjects: Apoptosis; Biochemistry; Biological Techniques; Biotechnology; Cell Biology; Cell cycle; Cell migration; Cell proliferation; Chemistry; Chemistry and Materials Science; Colon; Colon cancer; Colorectal cancer; Gene expression; Human Genetics; Original Paper; Phenotypes; Post-transcription; Protein expression; Protein Science; Proteins; Tumors
• ISSN: 1073-6085; 1559-0305
• DOI: 10.1007/s12033-022-00515-y

Accumulating studies have demonstrated that CADM2 modulated malignant phenotype of various cancer cells, while its regulatory function and mechanism have not yet been reported. In this study, qRT-PCR was utilized to measure CADM2 mRNA level in normal cells and colon cancer cells, also, IHC and WB were applied to detect CADM2 protein expression in colon tissues, exhibiting low mRNA and protein levels of CADM2 in colon cancer. Applying cell function experiments, the impacts of CADM2 on colon cell phenotypes were examined, and the results illustrated that upregulating CADM2 remarkably repressed proliferation, invasion, migration, cell cycle of colon cancer cells, and facilitated cell apoptosis. Thus, it could be considered that CADM2 served as a tumor repressor gene in colon cancer. Moreover, the outcomes of dual-luciferase assay displayed that miR-17-5p could target CADM2, and overexpressing miR-17-5p could notably inhibit the mRNA and protein expression levels of CADM2. We, therefore, assumed that CADM2 was a downstream target of miR-139-5p. qRT-PCR was conducted to assess miR-17-5p level in colon cancer cells and normal cells, verifying a high miR-17-5p expression in the cancer cells. The effects of miR-17-5p on colon cell phenotypes were examined as well, where we determined that miR-17-5p served as a tumor-promoting factor. Finally, the rescue experiments exhibited that miR-17-5p could activate tumor-promoting phenotypes, while such activating effects could be reversed by upregulating CADM2. In short, the study proved that miR-17-5p facilitated malignant progression of colon cancer through targeting CADM2 at a post-transcriptional level. Our findings offer new insight into molecular therapy of colon cancer patients.