Fig. 6: Combined Ref-1 redox inhibitor and vemurafenib treatment induced autophagic flow overload and caused senescence in BCPAP and K-1 cells. | Cell Death & Disease

Fig. 6: Combined Ref-1 redox inhibitor and vemurafenib treatment induced autophagic flow overload and caused senescence in BCPAP and K-1 cells.

From: Pharmacological inhibition of Ref-1 enhances the therapeutic sensitivity of papillary thyroid carcinoma to vemurafenib

Fig. 6

A Representative electron micrographs of BCPAP and K-1 cell lines. The green arrows indicate lysosome and the red arrows indicate autophagosome. B Immunofluorescence detection of the autophagic substrates LC3B and p62 in BCPAP and K-1 cell lines. C Western blot detection of the autophagic substrates LC3B and p62 in BCPAP and K-1 cell lines. D Cellular senescence detection by β-galactosidase staining in BCPAP and K-1 cell lines. E Immunofluorescence detection of γH2AX in BCPAP and K-1 cell lines. F Western blot detection of the autophagic substrates LC3B and p62 in BCPAP and K-1 cell lines. G Cellular senescence detection by β-galactosidase staining in BCPAP and K-1 cell lines. BCPAP and K-1 cell lines in A–E were pretreated with DMSO, vemurafenib (10 μM), E3330 (50 μM), and combination (10 μM vemurafenib + 50 μM E3330), respectively. BCPAP and K-1 cell lines in F, G were pretreated with DMSO, combination (10 μM vemurafenib + 50 μM E3330), HCQ, and combination + HCQ, respectively.

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