Fig. 8: An SLC2A3-neutralizing antibody enhances the antineoplastic effect of sorafenib on HGSOC patient-derived xenograft tumors with low OSGIN1 expression.
From: A targetable OSGIN1 − AMPK − SLC2A3 axis controls the vulnerability of ovarian cancer to ferroptosis
a Representative IHC staining images of tumor tissues collected from NSG mice bearing PDX models. Scale bar: 50 μm. All the data are expressed as the means ± SDs. b Model for the role of the OSGIN1−AMPK−SLC2A3 axis in ferroptosis. Loss of the OSGIN1 gene promoted the growth of ovarian cancer and induced resistance to drug-induced ferroptosis. Mechanistically, the loss of OSGIN1 activates AMPK signaling through ATM, leading to the upregulation of SLC2A3, which protects cells from ferroptosis and renders them insensitive to ferroptosis inducers. c, d Tumor growth curves and Kaplan−Meier survival curves of NSG mice bearing PDX models. Mice were treated with anti-SLC2A3 antibodies and sorafenib, either alone or in combination (n = 8). The survival time of the tumor-bearing mice was determined. Statistical significance was determined by a two-tailed unpaired t-test a and log-rank test c. Error bars are s.e.m. *p < 0.05; **p < 0.01 and ***p < 0.001.
