Journal: iScience
Article Title: IPO5 contributes to cetuximab resistance in colorectal cancer by modulating Ras signaling
doi: 10.1016/j.isci.2026.117714
Figure Lengend Snippet: The overexpression of IPO5 attenuates the cetuximab-mediated inhibition of Ras signaling (A) Subcellular fractionation and densitometric quantification of RASAL2 in cytoplasmic (Cyt) and nuclear (Nuc) fractions of RKO and LoVo cells following IPO5 knockdown or overexpression (lamin B and GAPDH served as fraction controls). (B) GST-Raf1-RBD pull-down assay assessing active Ras-GTP levels in CRC cells upon IPO5 modulation. (C) Rescue GST pull-down assays evaluating Ras-GTP levels in Caco2 and LoVo cells co-transfected with IPO5 and wild-type (WT) or NLS-mutant (Mut) RASAL2. (D) Western blot analysis and quantification of downstream proteins (p-AKT, AKT, p-MEK, MEK1/2, p-ERK, and ERK1/2) in cetuximab-treated cells under IPO5 modulation. (E) CCK-8 cell viability curves of Caco2 and LoVo cells treated with cetuximab following co-transfection of IPO5 with RASAL2-NLS-WT or NLS-Mut. Data are presented as mean ± SD ( n = 3 independent experiments). Statistical significance was determined using an unpaired two-tailed Student’s t test (A and B), one-way ANOVA with Tukey’s test (C), or two-way ANOVA with Tukey’s test (D and E). Exact p values are indicated.
Article Snippet: Caco2 , ATCC , Cat# HTB-37.
Techniques: Over Expression, Inhibition, Cell Fractionation, Knockdown, Pull Down Assay, GST Pulldown Assay, Transfection, Mutagenesis, Western Blot, Analysis, CCK-8 Assay, Cotransfection, Two Tailed Test