Journal: Frontiers in Immunology

Article Title: Inhibition of CRM1 reverses hypoxia-driven chemoresistance in acute myeloid leukemia via overcoming HIF-1α-mediated lysosomal sequestration

doi: 10.3389/fimmu.2025.1710230

Figure Lengend Snippet: CRM1 regulates HIF-1α by altering the subcellular localization of PHD2 in hypoxia. (A) Western blot analysis demonstrated that the expression of PHD2 and CRM1 in MV4–11 cells increased in hypoxia in a time-dependent manner. (B, C) Immunofluorescence analysis of PHD2 subcellular localization revealed the proportion of MV4–11 cells exhibiting nuclear accumulation of PHD2 decreased in hypoxia. (D) Protein expression levels of PHD2, CRM1, and HIF-1α in MV4–11 cells treated with or without Selinexor(0.1μM, 0.5μM). (E, F) Nuclear accumulation of PHD2 in MV4–11 cells treated with or without Selinexor (0.1μM, 0.5μM) in hypoxia. * indicates p<0.05, **p<0.01, ***p<0.001, ****p<0.0001.

Article Snippet: The membranes were then blocked with 5% bovine serum albumin (BSA) in Tris-buffered saline with Tween (TBST) for 1 hour and incubated with specific primary antibodies: anti-PHD2 antibody (1:1000, NB100-137), anti-HIF-1a antibody (1:1000, Cell Signaling), anti-P-gp antibody (1:1000, Cell Signaling), anti-CRM1 antibody (1:1000, Cell Signaling), and anti-GAPDH (1:1000, Proteintech) at 4°C overnight.

Techniques: Western Blot, Expressing, Immunofluorescence