Short Chain Fatty Acid Sodium Butyrate Increases miR-21, miR-143 and miR-145 Expression in Human Colorectal Cancer...

Area of Science:

• Molecular Biology
• Epigenetics
• Cancer Research

Background:

• Sodium butyrate (NaBu) is a short-chain fatty acid and a known histone deacetylase inhibitor.
• Histone deacetylase inhibitors can modulate genetic and epigenetic gene expression.
• Colorectal cancer (CRC) is a significant global health concern with complex molecular underpinnings.

Purpose of the Study:

• To investigate the effect of NaBu on the expression of specific microRNAs (miRNAs) in human colorectal cancer cells.
• To elucidate the potential of NaBu as an adjuvant therapy in CRC treatment.

Main Methods:

• Human colorectal cancer HCT-116 cell lines were treated with varying concentrations of NaBu (6.25 mM to 200 mM) over 24, 48, and 72 hours.
• Cytotoxicity was assessed using the MTT assay to determine IC50 values.
• Quantitative Real-Time-PCR (qRT-PCR) was employed to measure the expression levels of miR-21, miR-143, and miR-145.

Main Results:

• MTT assay revealed IC50 values for HCT-116 cells at 50 mM (24h), 12.5 mM (48h), and 6.25 mM (72h).
• qRT-PCR demonstrated a significant up-regulation of miR-21, miR-143, and miR-145 expression at specific NaBu concentrations and time points (P<0.05).
• Significant upregulation was observed with 50 mM NaBu at 24h, 12.5 mM at 48h, and 6.25 mM at 72h.

Conclusions:

• The observed upregulation of miR-21, miR-143, and miR-145 is likely mediated by transcriptional regulation and histone acetylation.
• NaBu's ability to modulate miRNA expression suggests its potential as a therapeutic agent in colorectal cancer.
• NaBu may represent a promising strategy to enhance existing histone deacetylase inhibitor-based therapies for colon cancer.