Fig. 3: HR-proficient ovarian tumors exhibit elevated levels of MGAT5, the enzyme that catalyzes branched N-glycans, compared to HR-deficient tumors.

a The glycan structures PHA-E (left) and PHA-L (right) are specific for branched N-glycans that are catalyzed by the MGAT5 enzyme. b HR-proficient cell lines PEO4 and OVCAR3 expressing shMGAT5 and shControl were validated for MGAT5 knockdown by immunoblot (left panels) and examined for the frequency of PHA-L binding to the cells (right panels). P-values were calculated using two-tailed t-test. n = 3 biologically independent samples. Error bars represent mean with SD. c Kaplan–Meier analysis of overall survival (OS) based on MGAT5 mRNA levels in the TCGA HGSOC database. n = 373 patients. Quartile-grouping (low, high) was chosen in the analysis. P-value was calculated by Log-rank test. d Relative expression of MGAT5 mRNA in HR-proficient (UPK10 and ID8) versus HR-deficient (BPPNM and HGS2) cells. n = 3 biologically independent samples. P-values were calculated using non-parametric two-tailed t-test. e Expression of MGAT5 protein in HR-proficient cell lines and HR-deficient cell lines of mouse (right) and human (left). P-values were calculated using two-tailed t-test. f Cell cycle distribution as determined by FACS analysis in the indicated BPPNM and PPNM cells. n = 3 biologically independent samples. Error bars represent mean with SEM. P-values were calculated using two-tailed t-test. g Positive Spearman’s r correlations (two-tailed) between MGAT5 and BRCA1/2 expression in 1139 BRCA1/2 wildtype cancer cell lines across cancer types in the Cancer Cell Line Encyclopedia RNAseq database. h Positive Spearman’s r correlations (one-tailed) between MGAT5 and BRCA1/2 expression in 236 HGSOC tumors with wildtype BRCA1/2 in the TCGA dataset. i Mutual exclusivity between MGAT5 amplification and/or overexpression and genetic alterations in the HR pathway in the TCGA HGSOC dataset. n = 201 patients. P-value was calculated using one tailed hypergeometric test. j MGAT5 is expressed at significantly higher levels in HGSOC tumors with wildtype genes of the HR pathway (n = 160) versus HGSOC tumors with driver mutations in HR pathway genes (n = 22) in the TCGA HGSOC dataset. One-tailed P-value was calculated by non-parametric t-test. Error bars represent median with IQR. Source data are provided as a Source Data file.