Sodium butyrate induces human colon carcinoma HT-29 cell apoptosis through a mitochondrial pathway

L Wang1, H-S Luo, H Xia

  • 1Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China.

Insights

Sodium butyrate (NaBt) effectively triggers apoptosis in human colon cancer cells. This process involves mitochondrial pathways and enhances caspase-3 and caspase-9 activity, offering a new therapeutic avenue beyond tumor necrosis factor-alpha (TNF-alpha).

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Tumor necrosis factor-alpha (TNF-alpha) shows promise in cancer treatment, but resistance limits its efficacy.
  • Alternative pathways for inducing apoptosis are crucial for overcoming treatment resistance.
  • Sodium butyrate (NaBt) exhibits anti-cancer properties, including growth inhibition, differentiation, and apoptosis induction in colon cancer.

Purpose of the Study:

  • To investigate the induction of apoptosis by Sodium butyrate (NaBt) in the human colon cancer cell line HT-29.
  • To elucidate the intracellular mechanisms underlying NaBt-induced apoptosis.

Main Methods:

  • Human colon cancer cell line HT-29 was treated with Sodium butyrate (NaBt).
  • Apoptosis was assessed using fluorescence activated cell sorter (FACS) analysis and mitochondrial membrane potential determination.
  • The role of caspases was evaluated using specific caspase inhibitors (z-VAD-fmk, z-DEVD-fmk, z-LEHD-fmk, z-IETD-fmk).

Main Results:

  • Sodium butyrate (NaBt) significantly increased apoptosis in HT-29 cells.
  • NaBt-induced apoptosis was inhibited by pan-caspase, caspase-3, and caspase-9 inhibitors, but not by a caspase-8 inhibitor.
  • Enhanced activity of caspase-3 and caspase-9 was observed following NaBt treatment.

Conclusions:

  • Sodium butyrate (NaBt) effectively induces apoptosis in human colon cancer cells.
  • The mechanism involves the mitochondrial pathway and activation of caspase-3 and caspase-9.
  • NaBt represents a potential therapeutic agent for colon cancer, acting independently of the TNF-alpha pathway.

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