期刊
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
卷 -, 期 -, 页码 -出版社
WILEY
DOI: 10.1002/jbt.23585
关键词
apoptosis; autophagy; head and neck squamous cell carcinoma; NF-kappa B p65; Schisandrin B
The study found that Schisandrin B (Sch B) exerts anticancer effects on head and neck squamous cell carcinoma (HNSCC) by regulating apoptosis and autophagy. Sch B can induce apoptosis and autophagy in HNSCC cells, and inhibition of autophagy can enhance the apoptotic effect of Sch B. Additionally, Sch B-activated autophagy in HNSCC cells is dependent on the nuclear factor-kappa B (NF-kappa B) pathway, and reactive oxygen species (ROS) act as a regulator of the NF-B pathway. Therefore, inhibiting autophagy to enhance the anticancer effect of Sch B deserves further research.
Head and neck squamous cell carcinoma (HNSCC) is among the most common malignant tumors worldwide and has a poor prognosis. Autophagy regulation has been proposed as a possible treatment option for HNSCC. Schisandrin B (Sch B) exerts anticancer effects by regulating apoptosis and autophagy, but the anticancer effect of Sch B in HNSCC remains unclear. This study aimed to investigate the effects of Sch B on human Cal27 HNSCC cells and to further reveal its potential regulatory mechanisms. The anticancer effect of Sch B was evaluated in vitro by flow cytometry, clonogenic assays, and Western blot analysis. The regulatory mechanism of Sch B-induced apoptosis and autophagy was further explored by polymerase chain reaction, luciferase assay, and reactive oxygen species (ROS) detection. The results showed that Sch B significantly induced apoptosis and autophagy in Cal27 cells and that inhibition of autophagy enhanced the apoptotic effect of Sch B on Cal27 cells. Additionally, Sch B-activated autophagy in Cal27 cells was dependent on the nuclear factor-kappa B (NF-kappa B) pathway, and ROS acted as a regulator of the NF-B pathway. N-acetylcysteine, a scavenger of ROS, inhibited Sch B-dependent autophagy via the NF-kappa B pathway. Based on the results, Sch B is a potential therapeutic agent for HNSCC and activates the NF-kappa B pathway by increasing ROS production, which subsequently promotes autophagy in HNSCC cells. Therefore, the strategy of enhancing the anticancer effect of Sch B by inhibiting autophagy deserves further attention.
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