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Butyrate induces ROS-mediated apoptosis by modulating miR-22/SIRT-1 pathway in hepatic cancer cells
Kishor Pant1, Ajay K Yadav1, Parul Gupta1
1Faculty of Life Sciences and Biotechnology, South Asian University, Chanakyapuri, New Delhi, India.
Abstract:
Butyrate is one of the short chain fatty acids, produced by the gut microbiota during anaerobic fermentation of dietary fibres. It has been shown that it can inhibit tumor progression via suppressing histone deacetylase and can induce apoptosis in cancer cells. However, the comprehensive pathway by which butyrate mediates apoptosis and growth arrest in cancer cells still remains unclear. In this study, the role of miR-22 in butyrate-mediated ROS release and induction of apoptosis was determined in hepatic cells. Intracellular expression of miR-22 was increased when the Huh 7 cells were incubated with sodium butyrate. Over-expression of miR-22 or addition of sodium butyrate inhibited SIRT-1 expression and enhanced the ROS production. Incubation of cells with anti-miR-22 reversed the effects of butyrate. Butyrate induced apoptosis via ROS production, cytochrome c release and activation of caspase-3, whereas addition of N-acetyl cysteine or anti-miR-22 reversed these butyrate-induced effects. Furthermore, sodium butyrate inhibited cell growth and proliferation, whereas anti-miR-22 inhibited these butyrate-mediated changes. The expression of PTEN and gsk-3 was found to be increased while p-akt and β-catenin expression was decreased significantly by butyrate. These data showed that butyrate modulated both apoptosis and proliferation via miR-22 expression in hepatic cells.
Insights
Sodium butyrate, a fiber fermentation product, induces cancer cell apoptosis and growth arrest. This study reveals butyrate
Area of Science:
- Hepatology
- Molecular Biology
- Cancer Research
Background:
- Butyrate, a short-chain fatty acid from dietary fiber fermentation, exhibits anti-tumor properties by inducing apoptosis.
- The precise molecular mechanisms by which butyrate mediates apoptosis and growth arrest in cancer cells remain incompletely understood.
Purpose of the Study:
- To investigate the role of microRNA-22 (miR-22) in butyrate-induced reactive oxygen species (ROS) production and apoptosis in hepatic cells.
- To elucidate the signaling pathways modulated by butyrate and miR-22 in liver cancer cells.
Main Methods:
- Hepatic cells (Huh 7) were treated with sodium butyrate and/or anti-miR-22.
- Assessed intracellular miR-22 expression, SIRT-1 levels, ROS production, apoptosis markers (cytochrome c, caspase-3), cell proliferation, and key signaling proteins (PTEN, gsk-3, p-akt, β-catenin).
Main Results:
- Sodium butyrate increased intracellular miR-22 expression and ROS production, while inhibiting SIRT-1.
- Butyrate induced apoptosis via ROS, cytochrome c release, and caspase-3 activation, effects reversed by N-acetyl cysteine or anti-miR-22.
- Butyrate inhibited cell proliferation and modulated PTEN, gsk-3, p-akt, and β-catenin signaling, with anti-miR-22 reversing these effects.
Conclusions:
- Butyrate modulates apoptosis and proliferation in hepatic cells through miR-22-dependent pathways.
- miR-22 plays a critical role in mediating butyrate's effects on ROS production, apoptosis, and cell growth inhibition.
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