China Journal of Oral and Maxillofacial Surgery ›› 2023, Vol. 21 ›› Issue (2): 105-111.doi: 10.19438/j.cjoms.2023.02.001

• Original Articles • Previous Articles     Next Articles

Effect of docetaxel on cell pyroptosis of head and neck squamous cell carcinoma and its mechanism

GAO Jia-min, YAO Yan-li, WANG Yu-jue, ZHANG Zhi-yuan, SUN Shu-yang   

  1. Department of Oromaxillofacial Head and Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine; College of Stomatology, Shanghai Jiao Tong University; National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology; Shanghai Research Institute of Stomatology. Shanghai 200011, China
  • Received:2022-10-17 Revised:2022-12-26 Online:2023-03-20 Published:2023-06-12

Abstract: PURPOSE: To explore the effect of docetaxel on pyroptosis of head and neck squamous carcinoma and the underlying molecular mechanism. METHODS: Head and neck squamous carcinoma cell lines (CAL33 and SCC154) were treated with control group(0 μmol/L) and different concentrations of docetaxel (0.625, 1.25, 2.5, 5 and 10 μmol/L). The morphological change of cell proptosis was observed by living cell workstation. Western blot was used to assess the protein expression of GSDME, GSDME-N terminal, caspase-3 and cleaved caspase-3. The expression of caspase-3 in living cells was monitored by Caspase-3 Activity and Apoptosis Detection Kit for Live Cell. The level of reactive oxygen species(ROS) was quantified by Reactive Oxygen Species Assay Kit. To determine whether the inhibition of ROS had an effect on pyroptosis induced by docetaxel, acetylcysteine (NAC) was used to inhibit the ROS accumulation and the protein expression of GSDME and GSDME-N terminal of control group(0 μmol/L) was tested, group of docetaxel (2.5 μmol/L) without NAC(5 mmol/L), group of docetaxel with NAC and group of NAC without docetaxel by Western blot. SAS 9.4 software package was used for data analysis. RESULTS: Compared with the control group, docetaxel induced cell pyroptosis of CAL33 and SCC154, which was characterized by membrane rupture and surface protrusions. Docetaxel also promoted caspase-3 activity in the living cells, while the GSDME-N terminal and Cleaved-caspase-3 were upregulated(P<0.05). The level of ROS was increased by docetaxel, and high expression of GSDME-N terminal was significantly reversed by acetylcysteine(P<0.05). CONCLUSIONS: Docetaxel may induce pyroptosis of head and neck squamous carcinoma cells by activating ROS/Caspase-3/GSDME pathway.

Key words: Docetaxel, Head and neck squamous cell cancer, Cell pyroptosis, Caspase-3, GSDME

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