Research Paper Volume 16, Issue 1 pp 627—647
Targeting of FSP1 regulates iron homeostasis in drug-tolerant persister head and neck cancer cells via lipid-metabolism-driven ferroptosis
Figure 3. Overexpression of FSP1 enhanced cellular function in HSC cells and was reversed by FSP1 inhibitor. (A) Overexpression of FSP1 in the transfected HSC cell line. (B) Diameter of tumor spheres. (C) RNA analysis of related genes of HSC DTP cells through FSP1 inhibitor treatment. (D) HSC DTP cells were compared with parental counterparts in terms of their sensitivity to cisplatin, FSP1 inhibitor, and combination treatment. (E) Western blotting indicated the expression levels of iron-metabolism-related markers FSP1, IREB2, FBXL5, and GPX4; fatty acid metabolism marker ACSL4; and antioxidant marker SOD2 in HSC DTP cells. Actin was used as a loading control. (F) Downregulation of lipid components following FSP1 inhibition. (G) Potential regulatory network of ferroptosis in cells, involving three pathways: ferroptosis, fatty acid metabolism, and cellular antioxidation. (*p < 0.05, **p < 0.01, ***p < 0.001). Scale bar: 5 μm.