Fig. 6: 1,25D inhibits claudin1/AKT/cancer cell stemness pathway by inhibiting β-catenin activation. | Cell Death Discovery

Fig. 6: 1,25D inhibits claudin1/AKT/cancer cell stemness pathway by inhibiting β-catenin activation.

From: Claudin1 decrease induced by 1,25-dihydroxy-vitamin D3 potentiates gefitinib resistance therapy through inhibiting AKT activation-mediated cancer stem-like properties in NSCLC cells

Fig. 6

A, B PC9/GR and H1975 cells were stimulated with various concentrations of SKL2001 for 24 h, then the expression levels of claudin1, Nanog, Oct4, Sox2, and ALDH1A1 were determined. C PC9/GR and H1975 cells were treated with various concentrations of 1,25D after which β-catenin level was determined by western blotting. D, E Nuclear and cytoplasmic fractions of PC9/GR and H1975 cells in the presence or absence of 1,25D were prepared, and VDR and β-catenin expression levels were determined by western blotting. GAPDH and Histone-H3 were, respectively, used as cytoplasm and nucleus loading controls. F Expression levels of claudin1 were determined after PC9, PC9/GR, H1975, and H1650 cells were treated with DMSO, 1,25D (100 nM), or EB (100 nM) for 48 h. G Relative mRNA expression levels of CLDN1 were detected by real-time PCR after PC9, PC9/GR, H1650, and H1975 cells had been treated with 1,25D or EB (mean ± SD; n = 6; *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001). H–J PC9, PC9/GR, and H1975 cells were treated with various concentrations of 1,25D, respectively, for 24 and 48 h after which claudin1 protein expression was evaluated. K, L PC9/GR and H1975 cells were treated with DMSO, 1,25D (100 nM), or EB (100 nM) for 48 h, then the expression levels of VDR, ALDH1A1, Nanog, Oct4, and Sox2 were evaluated by western blotting. M, N PC9/GR and H1975 cells were, respectively, treated with 1,25D, SKL2001, or a combination of 1,25D and SKL2001, and the expression levels of β-catenin, claudin1, p-AKT, Sox2, and ALDH1A1 were determined.

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