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Apigenin induces apoptosis in human lung cancer H460 cells through caspase- and mitochondria-dependent pathways
Hsu-Feng Lu1, Yu-Jie Chie, Ming-Sung Yang
1Department of Clinical Pathology, Cheng Hsin General Hospital, Taipei, Taiwan.
Abstract:
Apigenin (4,5,7-trihydroxyflavone), a promising chemopreventive agent presented in fruits and vegetables, has been shown to induce cell cycle arrest and apoptosis in many types of human cancer cell lines. However, there is no available information to address the effects of apigenin on human lung cancer H460 cells. In the present studies, H460 cells were treated with apigenin for different time and then were analyzed for the morphological changes, induction of apoptosis, protein levels associated with apoptosis and results in dose-dependent induction of morphological changes, decrease in the percentage of viability, induced DNA damage and apoptosis; down-modulation of the protein expression of Bid, Bcl-2, procaspase-8; up-regulation of protein levels of Bax, caspase-3, AIF, cytochrome c, GRP78 and GADD153; decreased the levels of mitochondrial membrane potential and increased the productions of reactive oxygen species (ROS) and Ca(2+) in H460 cells. Taken together, this is the first systematic in vitro study showing the involvement of apoptosis regulatory proteins as potential molecular targets of apigenin in human lung cancer H460 cells.
Insights
Apigenin induces apoptosis and DNA damage in human lung cancer H460 cells. This study reveals apigenin
Area of Science:
- Molecular Biology
- Cancer Research
- Biochemistry
Background:
- Apigenin, a natural flavonoid found in fruits and vegetables, exhibits chemopreventive properties.
- Previous studies indicate apigenin induces cell cycle arrest and apoptosis in various cancer cell lines.
- Limited information exists regarding apigenin's effects on human lung cancer H460 cells.
Purpose of the Study:
- To investigate the in vitro effects of apigenin on human lung cancer H460 cells.
- To elucidate the molecular mechanisms underlying apigenin-induced apoptosis in H460 cells.
Main Methods:
- H460 cells were treated with varying concentrations and durations of apigenin.
- Morphological changes, cell viability, DNA damage, and apoptosis were assessed.
- Protein levels of apoptosis-related factors (Bid, Bcl-2, Bax, caspase-3, AIF, cytochrome c, GRP78, GADD153, procaspase-8) were analyzed.
- Mitochondrial membrane potential, reactive oxygen species (ROS), and intracellular calcium (Ca2+) levels were measured.
Main Results:
- Apigenin treatment resulted in dose-dependent morphological changes, decreased cell viability, and induced DNA damage and apoptosis.
- Apigenin modulated key apoptosis regulatory proteins, including down-regulation of Bid, Bcl-2, and procaspase-8, and up-regulation of Bax, caspase-3, AIF, and cytochrome c.
- Apigenin decreased mitochondrial membrane potential and increased ROS and Ca2+ production in H460 cells.
Conclusions:
- This study provides the first systematic in vitro evidence of apigenin's anti-cancer effects on human lung cancer H460 cells.
- Apigenin induces apoptosis in H460 cells through the modulation of apoptosis regulatory proteins.
- Apigenin's molecular targets include proteins involved in apoptosis pathways, making it a potential therapeutic agent for lung cancer.
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