Fig. 7: The oncogenic roles of BUD31 in ovarian cancer partially rely on BCL2L12 expression.

a Correlation analysis of mRNA expression between BUD31 and BCL2L12 in SOCs and normal ovaries from the TCGA-OV and GTEx datasets. (Pearson’s r = 0.39). b Western blot analysis of BCL2L12 protein expression in HEYA8 cells with BUD31 knockdown or overexpression in A2780 cells. Protein expression was quantified and normalized with the control group. c Immunoblot analysis of BUD31 and BCL2L12 protein levels in HEYA8 cells transfected with shBUD31 or BCL2L12 overexpression vector. Apoptosis (d), clonogenic (e), and EdU (f) assays for investigating the potential of BCL2L12 to rescue the loss of BUD31 in terms of apoptosis and proliferation. g–i Xenograft experiments by subcutaneous injection were conducted in HEYA8 cells with dox-inducible BUD31 knockdown or BCL2L12 overexpression vector. Representative image (g), volume curves (h), and weight (i) of xenograft tumors showed that BCL2L12 could partially rescue the inhibitory effect of BUD31 on tumor growth (n = 10). j BCL2L12 expression was analyzed in SOCs from TCGA-OV (n = 374) and in normal ovaries from GTEx (n = 180). k BCL2L12 mRNA expression was determined by qPCR in SOC (n = 23) and FT (n = 9) samples. l Kaplan–Meier analysis of BCL2L12 expression on the overall survival of ovarian cancer patients based on cohorts from Kaplan–Meier Plotter. The high and low-expression groups were separated based on the auto-select cutoff. All functional experiments were performed with n = 3 biological repeats. The p values were determined by a two-tailed unpaired Student’s t-test (d, e, f, h, i, j, k), or log-rank test (l), and the results are presented as the mean ± SD. *p < 0.05, **p < 0.01. Source data are provided as a Source Data file.