法托他汀通过靶向SCAP/SREBP通路促进铁死亡及抑制ARID1A缺失型非小细胞肺癌

陈鑫鸿, 张雪, 刘婷, 张淑敏, 马雨鹏, 来佳辉, 章子晗, 池永斌

Fatostatin targets SCAP/SREBP pathway to inhibit ARID1A-deficient non-small cell lung cancer by promoting ferroptosis

Chen Xinhong, Zhang Xue, Liu Ting, Zhang Shumin, Ma Yupeng, Lai Jiahui, Zhang Zihan, Chi Yongbin

图4 法托他汀对 ARID1A 敲除NSCLC细胞铁死亡的诱导作用 Note： A. KEGG enrichment map of cell growth- and death-related pathways between ARID1A-KO and WT A549 cells. B. Viability of ARID1A-KO cells treated with fatostatin (10 μmol·L-1, 24 h) with or without deferoxamine (DFO, 100 μmol·L-1, 2 h) pretreatment. C/D. Western blotting analysis of ferroptosis markers after fatostatin treatment (10 μmol·L-1, 24 h) (C) and densitometric quantification (D). E/F. Representative JC-1 staining images (E) and red/green fluorescence intensity ratios (F) of mitochondrial membrane potential in A549 WT cells after fatostatin treatment. G/H. Representative JC-1 staining images (G) and red/green fluorescence intensity ratios (H) in ARID1A-KO A549 cells after fatostatin treatment. CCCP—carbonyl cyanide m-chlorophenylhydrazone.

Fig 4 Fatostatin-induced ferroptosis in ARID1A-knockout NSCLC cells