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Inhibiting reactive oxygen species-dependent autophagy enhanced baicalein-induced apoptosis in oral squamous cell
Bo Li1, Mei Lu1, Xin-Xiang Jiang1
1Department of Oral and Maxillofacial Surgery, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi Zhuang Autonomous Region, People's Republic of China.
Abstract:
Autophagy modulation has been considered a potential therapeutic strategy for oral squamous cell carcinoma (OSCC). A previous study confirmed that baicalein might possess significant anti-carcinogenic activity. However, whether baicalein induces autophagy and its role in cell death in OSCC are still unclear. The aim of this study was to investigate the anticancer activity and molecular targets of baicalein in OSCC in vitro. In this study, we found that baicalein induced significant apoptosis in OSCC cells Cal27. In addition to showing apoptosis induction, we also demonstrated baicalein-induced autophagic response in Cal27 cells. Moreover, pharmacologically or genetically blocking autophagy enhanced baicalein-induced apoptosis, indicating the cytoprotective role of autophagy in baicalein-treated Cal27 cells. Importantly, we found that baicalein triggered reactive oxygen species (ROS) generation in Cal27 cells. Furthermore, N-acetyl-cysteine, a ROS scavenger, abrogated the effects of baicalein on ROS-dependent autophagy. Therefore, we found that baicalein increased autophagy through the promotion of ROS signaling pathways in OSCC. These data also suggest that a strategy of blocking ROS-dependent autophagy to enhance the activity of baicalein warrants further attention for the treatment of OSCC.
Insights
Baicalein triggers apoptosis and autophagy in oral squamous cell carcinoma (OSCC) cells. Blocking autophagy enhances baicalein
Area of Science:
- Oncology
- Cell Biology
- Biochemistry
Background:
- Autophagy modulation is a potential therapeutic strategy for oral squamous cell carcinoma (OSCC).
- Baicalein exhibits anti-carcinogenic properties, but its role in OSCC autophagy and cell death remains unclear.
Purpose of the Study:
- To investigate the anticancer effects of baicalein in OSCC.
- To elucidate the molecular mechanisms, including autophagy and reactive oxygen species (ROS) signaling, underlying baicalein's activity in OSCC cells.
Main Methods:
- In vitro study using OSCC Cal27 cells.
- Assessed apoptosis and autophagy induction by baicalein.
- Investigated the role of autophagy and ROS using pharmacological and genetic inhibition and ROS scavengers.
Main Results:
- Baicalein significantly induced apoptosis and autophagy in Cal27 cells.
- Inhibition of autophagy enhanced baicalein-induced apoptosis, suggesting a cytoprotective role for autophagy.
- Baicalein triggered ROS generation, which mediated the induction of autophagy.
Conclusions:
- Baicalein exhibits anticancer activity in OSCC by inducing apoptosis and autophagy.
- Autophagy acts protectively in baicalein-treated OSCC cells.
- Baicalein-induced autophagy is regulated by ROS signaling, suggesting a therapeutic strategy of combining baicalein with autophagy inhibitors for OSCC treatment.
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