Tissue & cell · 2026
FUNDC1 inhibition induces mitochondrial dysfunction and drives pyroptosis of gastric cancer cells mediated by Caspase 3/GSDME.
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Yu Panpan, Chen Jiahui, Shen Xingyuan, Jiang Zhengchen, Wan Xiuping, Wang Lijuan
Аннотация
OBJECTIVES: The incidence of gastric cancer (GC) has risen significantly. This study is to elucidate the function of FUNDC1 in the carcinogenesis of GC and its potential molecular mechanism, and to find a new target for the treatment of GC.
MATERIALS AND METHODS: The expression differences of FUNDC1 were analyzed using the UALCAN database, Real-time fluorescence quantitative PCR and Western blot (WB). Lentiviral vectors overexpressing and knocking down FUNDC1 were respectively transfected into GC cells. The cell proliferation and motility abilities were evaluated. The changes of mitochondrial autophagy and pyroptosis were explored by WB, flow cytometry and immunofluorescence assay. In addition, the GC cells with FUNDC1 knocked down were treated with ROS scavenger Acetylcysteine (NAC) to observe its effects on pyroptosis and biological behaviors.
RESULTS: FUNDC1 shows a significantly higher expression level in GC tissues and cell lines. Functional experiments show that overexpression of FUNDC1 markedly promotes the proliferation and motility of GC cells, while knockdown of FUNDC1 inhibits these abilities. FUNDC1 inhibition suppressed mitochondrial autophagy, induced mitochondrial dysfunction, and promoted the process of cell pyroptosis. Mechanism research found that the addition of NAC can reverse the pyroptosis, inflammatory factor release and cell viability inhibition induced by knockdown of FUNDC1, and restore the proliferation and motility of GC cells.
CONCLUSION: FUNDC1 promotes the occurrence and development of GC by regulating mitophagy, mitochondrial function and caspase 3/GSDME-mediated pyroptosis. FUNDC1 is expected to become a potential intervention target for the treatment of GC.
MATERIALS AND METHODS: The expression differences of FUNDC1 were analyzed using the UALCAN database, Real-time fluorescence quantitative PCR and Western blot (WB). Lentiviral vectors overexpressing and knocking down FUNDC1 were respectively transfected into GC cells. The cell proliferation and motility abilities were evaluated. The changes of mitochondrial autophagy and pyroptosis were explored by WB, flow cytometry and immunofluorescence assay. In addition, the GC cells with FUNDC1 knocked down were treated with ROS scavenger Acetylcysteine (NAC) to observe its effects on pyroptosis and biological behaviors.
RESULTS: FUNDC1 shows a significantly higher expression level in GC tissues and cell lines. Functional experiments show that overexpression of FUNDC1 markedly promotes the proliferation and motility of GC cells, while knockdown of FUNDC1 inhibits these abilities. FUNDC1 inhibition suppressed mitochondrial autophagy, induced mitochondrial dysfunction, and promoted the process of cell pyroptosis. Mechanism research found that the addition of NAC can reverse the pyroptosis, inflammatory factor release and cell viability inhibition induced by knockdown of FUNDC1, and restore the proliferation and motility of GC cells.
CONCLUSION: FUNDC1 promotes the occurrence and development of GC by regulating mitophagy, mitochondrial function and caspase 3/GSDME-mediated pyroptosis. FUNDC1 is expected to become a potential intervention target for the treatment of GC.