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Selenite induces redox-dependent Bax activation and apoptosis in colorectal cancer cells
Fang Huang1, Chunlai Nie, Yang Yang
1National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
Abstract:
Emerging evidence suggests that selenium has chemotherapeutic potential by inducing cancer cell apoptosis with minimal side effects to normal cells. However, the mechanism by which selenium induces apoptosis is not well understood. We have investigated the role of Bax, a Bcl-2 family protein and a critical regulator of the mitochondrial apoptotic pathway, in selenite-induced apoptosis in colorectal cancer cells. We found that supranutritional doses of selenite could induce typical apoptosis in colorectal cancer cells in vitro and in xenograft tumors. Selenite triggers a conformational change in Bax, as detected by the 6A7 antibody, and leads to Bax translocation into the mitochondria, where Bax forms oligomers to mediate cytochrome c release. Importantly, we show that the two conserved cysteine residues of Bax seem to be critical for sensing the intracellular ROS to initiate Bax conformational changes and subsequent apoptosis. Our results show for the first time that selenite can activate the apoptotic machinery through redox-dependent activation of Bax and further suggest that selenite could be useful in cancer therapy.
Insights
Selenium compounds, like selenite, can trigger cancer cell death (apoptosis) by activating the Bax protein. This redox-dependent mechanism offers potential for novel colorectal cancer therapies.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Selenium exhibits chemotherapeutic potential, inducing cancer cell apoptosis with minimal toxicity to normal cells.
- The precise mechanism of selenium-induced apoptosis, particularly involving key regulatory proteins, remains incompletely understood.
Purpose of the Study:
- To investigate the role of Bax, a critical regulator of mitochondrial apoptosis, in selenite-induced apoptosis in colorectal cancer cells.
- To elucidate the molecular mechanisms underlying selenite's apoptotic effects.
Main Methods:
- Treatment of colorectal cancer cells and xenograft tumors with supranutritional doses of selenite.
- Detection of Bax conformational changes using the 6A7 antibody.
- Assessment of Bax translocation to mitochondria and Bax oligomerization.
- Evaluation of cytochrome c release and reactive oxygen species (ROS) levels.
Main Results:
- Selenite induced apoptosis in colorectal cancer cells both in vitro and in vivo.
- Selenite triggered a Bax conformational change and its translocation to mitochondria.
- Bax oligomerization and subsequent cytochrome c release were observed.
- Two conserved cysteine residues in Bax were identified as critical for ROS sensing and initiating apoptosis.
Conclusions:
- Selenite activates the apoptotic machinery via redox-dependent activation of Bax.
- This study reveals a novel mechanism for selenite-induced apoptosis through Bax activation.
- Selenite demonstrates potential as a therapeutic agent for colorectal cancer treatment.
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