Fig. 3

EGOT induces autophagy to enhance paclitaxel sensitivity through ITPR1. a Western blot showing the effects of EGOT overexpression on LC3-II/LC3-I levels in HeLa (left) and UACC-812 cells (right) treated with CQ. b Western blot showing the effects of EGOT overexpression on LC3-II/LC3-I levels and P62 expression in HeLa (left) and UACC-812 cells (right) treated with EBSS. c Western blot showing the effects of EGOT overexpression on LC3-II/LC3-I levels in T47D cells treated with CQ. d Western blot showing the effects of EGOT overexpression on LC3-II/LC3-I levels and P62 expression in HeLa (left) and UACC-812 cells (right) treated with EBSS. e, f Confocal microscopy showing the effects of EBSS incubation on mRFP-GFP-LC3 distribution in HeLa EGOT overexpression cells (e) or T47D EGOT knockdown cells (f) 48 h after mRFP-GFP-LC3 adenovirus transfection (10,000× magnification). g, h Representative electron microscopy images and quantification of autophagic vacuoles in EGOT overexpression cells (g) and EGOT knockdown cells (h). Scale bar, 2 μm. Arrows depict autophagosomes, and the nucleus is denoted by N. i Representative hematoxylin and eosin (H&E), ITPR1, and LC3B staining of orthotopic xenograft sections from UACC-812 EGOT overexpression and control groups treated with or without paclitaxel. Scale bar, 400 μm. j Representative H&E, ITPR1 and LC3B staining in sections from 258 breast cancer tissues in HMUCC cohort. Scale bar, 200 μm. EGOT-H, EGOT-M, and EGOT-L represent high, medium, and low expression of EGOT, respectively. k Western blot showing LC3-II/LC3I levels in HeLa cells treated with CQ, different serum condition, EGOT overexpression or ITPR1 knockdown. Data are shown as the mean ± s.d. Student’s t-test was used for statistical analysis: * P < 0.05; ** P < 0.01; *** P < 0.001; and **** P < 0.0001. Data represent at least three independent experiments