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. 2019 Aug 12;9:11632. doi: 10.1038/s41598-019-48064-w

Figure 4.

Figure 4

SH3GL2 mediates rescue or abrogation of SPANXB1 expression and are physically associated with SPANXB1. (A) Silencing or overexpression of SH3GL2 (B) rescue or diminishes SPANXB1 expression in SPANXB1-KD or overexpressing cells respectively. (C) Bioinformatics analysis predicted possible interaction sites (green areas) between SPANXB1 and SH3GL2. (D) Co-IP analysis pulled down SPANXB1 with SH3GL2 or vice versa in SPANXB1 overexpressing HMLE cells. (E) High nuclear (black arrow) and cytoplasmic (red arrow) expression of SPANXB1 in primary cancer and matched lymph node metastatic tissues compared to normal controls (p = 0.0002–0.0001). Magnification x 200. (F,G) High SPANXB1 mRNA expression in overall BCa (p < 0.0001, (F)) and TNBC tissues (p < 0.0001, (G)) compared to normal in TCGA datasets, with distribution of data points plotted on top of box plots. Actin was used as a loading control. CSiRNA: Control SIRNA; SiRNA-SH3GL2: SH3GL2 targeted SiRNA pool. EV: Empty vector treated; SH3GL2: SH3GL2 transduced. In Western blotting, all experimental and control antibodies were run in parallel for the same immunoblot. The Image J software (https://imagej.nih.gov/ij/) was used for Western blot quantification.