Journal: iScience

Article Title: LAR1 promotes breast carcinogenesis by activating NF-κB signaling pathway through binding and enhancing APOC1 expression

doi: 10.1016/j.isci.2025.114386

Figure Lengend Snippet: LAR1 knockdown inhibited p65 nuclear translocation in BC cells (A) The protein expression of p -AKT (Ser473), AKT, p -IKK (Ser180/181), and IKK in MDA-MB-231 cells after LAR1 knockdown and overexpression. (B) The protein expression of p -IκBα (ser32/ser36), IκBα, p-p65 (Ser536), and p65 in MDA-MB-231 cells after LAR1 knockdown and overexpression. (C) Representative images of immunofluorescence staining for p65 in MDA-MB-231 cells after LAR1 knockdown and overexpression. Scale bars, 50 μm. (D) Quantitative analysis for the percentage of nuclear p65-positive cells in images of immunofluorescence staining ( n = 3). (E) Cell viability of MDA-MB-231 cells treated with PDTC (25 μmol/L) for 24 h was detected by CCK-8 assay. (F) Invasion of MDA-MB-231 cells treated with PDTC (25 μmol/L) for 24 h were visualized by Transwell assays ( n = 3). Scale bars, 100 μm. Data were presented as the mean ± SD, with statistical significance assessed using one-way ANOVA (for the left image of D, for E and 7F) or unpaired t test (for the right image of D). ∗∗ p < 0.01, the oeLAR1 group vs. the Vector group. # p < 0.05 and ## p < 0.01, the oeLAR1+PDTC group vs. the oeLAR1+Vehicle group.

Article Snippet: MDA-MB-231 cells were treated with the NF- κB inhibitor PDTC (25 μmol/L, Cat#A800469, Macklin Inc., Shanghai, China) for 24 h. For mRNA stability analysis, MDA-MB-231 cells were treated with 10 μg/mL actinomycin D (Cat#HY-17559, MCE, USA) for different periods of time (0, 1, 2, 3, or 4 h).

Techniques: Knockdown, Translocation Assay, Expressing, Over Expression, Immunofluorescence, Staining, CCK-8 Assay, Plasmid Preparation