MicroRNA-126 Inhibit Viability of Colorectal Cancer Cell by Repressing mTOR Induced Apoptosis and Autophagy

Area of Science:

• Oncology
• Molecular Biology
• Gene Regulation

Background:

• Colorectal cancer (CRC) is a significant cause of cancer-related mortality.
• Tumorigenesis involves complex cellular processes including proliferation, invasion, and migration.
• MicroRNA-126 (miR-126) has emerged as a key player in CRC tumorigenesis.

Purpose of the Study:

• To investigate the role of miR-126 in regulating cell viability, autophagy, and apoptosis in CRC.
• To elucidate the gene regulatory mechanisms influenced by miR-126 in CRC HCT116 cells.
• To explore the potential of miR-126 as a therapeutic target in CRC.

Main Methods:

• miRNA profiling of CRC and normal colorectal tissues.
• Real-time quantitative PCR and Western blot for RNA and protein analysis.
• MTT assays, colony formation assays, immunofluorescence, and Annexin V/PI flow cytometry to assess cell viability, autophagy, and apoptosis.

Main Results:

• miR-126 expression was significantly downregulated in CRC tissues and cell lines.
• Upregulation of miR-126 impaired CRC cell viability and growth, increased autophagy, and induced apoptosis.
• miR-126 directly targeted the mTOR gene, reducing its expression in CRC cells.
• Overexpression of mTOR counteracted the effects of miR-126 on autophagy and apoptosis.

Conclusions:

• miR-126 plays a critical role in regulating CRC cell activity through modulation of autophagy and apoptosis.
• A novel miR-126-mTOR interaction mechanism in CRC pathogenesis was identified.
• Targeting miR-126 presents a potential therapeutic strategy for colorectal cancer.