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. 2022 Nov 25;13(3):1053–1070. doi: 10.1016/j.apsb.2022.11.025

Figure 1.

Figure 1

HBXIP contributes to myosin-IIA disassembly and breast cancer migration. (A) The spatial distribution patterns of NMHC-IIA (red), F-actin (green) and nuclei (DAPI) were detected by IF. The filopodia were highlighted with yellow arrows. Scale bar, 20 μm. (B, C) Western blotting (WB) analysis showed Triton X-insoluble fractions of these cells with an anti-NMHC-IIA antibody and anti-β-actin antibody (B) and quantification of the intensity relative to the total lysate group (C). Total, total lysis; S, supernatant; P, pellet. (D) Kaplan–Meier plots of the disease-free survival rates of 814 metastatic breast cancer patients stratified according to the HBXIP mRNA levels from the TCGA dataset. (E, F) WB analysis showed Triton X-insoluble fractions of stably transfected cells with an anti-NMHC-IIA antibody (E) and quantification of the intensity relative to the total lysate group (F). (G) The spatial distribution patterns of NMHC-IIA (red) and nuclei (DAPI) were detected by IF. The elongated leading edges were highlighted with yellow arrows. Scale bar, 20 μm. (H–J) GSEA of breast cancer metastasis patients grouped by the mean expression value of HBXIP expression. Columns with error bars symbolize the average of three independent replicates ±SD. Three experiments with consistent results tendency were repeated by two-tailed Student's t test. ∗∗∗P < 0.001; ∗∗P < 0.01; ns, not significant.