miR-664b-3p inhibits colon cell carcinoma via negatively regulating Budding uninhibited by benzimidazole 3

• Published in: Bioengineered 2022-03, Vol.13 (3), p.4857-4868
• Main Authors: Zhao, Liang-Yu, Xin, Guo-Jun, Tang, Yuan-Yuan, Li, Xiao-Fei, Li, Yu-Zhen, Tang, Ning, Ma, Yu-Hong
• Format: Article
• Language: English
• Subjects: Apoptosis - genetics; BUB3 protein; Carcinoma - genetics; Cell Cycle Proteins - genetics; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; colon cancer; Colonic Neoplasms - genetics; Colonic Neoplasms - pathology; Gene Expression Regulation, Neoplastic; Humans; Ki-67 Antigen - genetics; Metalloproteases - genetics; MicroRNAs - genetics; miR-664b-3p; Poly-ADP-Ribose Binding Proteins - genetics; Research Paper
• ISSN: 2165-5979; 2165-5987
• DOI: 10.1080/21655979.2022.2036400

MiR-664b-3p has been reported to play a crucial role in cancer progression. This research explores the biological effect and molecular mechanisms of miR-664b-3p in cell proliferation, apoptosis, migration, and invasion of colon cancer. The expression level of miR-664b-3p and Budding uninhibited by benzimidazole 3 (Bub3) in colon cancer cell lines and tissues were detected and analyzed using quantitative real-time PCR and bioinformatics method. The Western blot measured the expression level of proliferation-related, migration-related, and apoptosis-related proteins. CCK-8 assessed cell viability, and the cell proliferation, migration, and invasion were detected by the Edu assay, wound-healing assay, and transwell assay, respectively. Annexin/propidium iodide (PI) assays detected apoptosis of cells. The target of miR-664b-3p was predicted by bioinformatics methods and then validated by gene engineering technology. MiR-664b-3p was downregulated in colon cancer tissues and cells. The cell proliferation, migration, and invasion of cells were inhibited after transfecting by miR-664b-3p mimics, whereas apoptosis was promoted. Over-expression of miR-664b-3p could reduce the expression of proliferation-promoted proliferating cell nuclear antigen (PCNA), proliferation marker protein Ki-67 (Ki-67), migration-promoted Cyclooxygenase-2 (COX-2), Matrix Metallopeptidase 2 (MMP-2), and Matrix Metallopeptidase 9 (MMP-9), and apoptosis-inhibited protein (Bcl-2) while increasing the expression of apoptosis-promoted BCL2-Associated X Protein (Bax), caspase-3, and caspase-9 proteins. The study indicated that miR-664b-3p plays a significant role in colon cancer and could regulate the progression of colon cancer tumor growth by suppressing the expression of BUB3 protein. These findings provide a novel strategy to screen and treat colon cancer.