Fig. 8: DCAF13 promotes tumor growth via global activation of translation.

a, b CCK8 assay (a) and colony formation assay (b) conducted on MDA-MB-231 and MDA-MB-468 cells following the overexpression of DCAF13 (n = 3 biological replicates). c Colony formation assay of MDA-MB-231 cells transfected with either siNC or siRPA194 alone, and included cells transfected with the EV, FN-RPA194-WT, or FN-RPA194-K1180/1184 R plasmid respectively in combination with siRPA194 (n = 3 biological replicates). d, e Flow cytometry analyses assessing cell cycle alterations (d) and apoptotic events (e) in MDA-MB-231 and MDA-MB-468 cells after knocking down DCAF13 (n = 3 biological replicates). f Representative images depicting resected tumors harvested from BALB/c nude mice, which were inoculated with MDA-MB-231 cells stably expressing either the Empty Vector (control), WT DCAF13, shNC (control), or shDCAF13 plasmids. g, h Longitudinal measurements of tumor volumes collected at predetermined intervals (n = 8/group for EV/oe-DCAF13, n = 9/group for shNC/shDCAF13). i The weights of the excised tumors recorded at the designated end point of the study (n = 6/group for EV/oe-DCAF13, n = 7/group for shNC/shDCAF13). j Schematic model of this study drawn by eBioart of Guangzhou Guorenqidian Shengwukeji Co., Ltd. DCAF13 facilitates K63-linked ubiquitination of RPA194, which can be removed by USP36. The elevated expression of DCAF13 in BC leads to hyper-ubiquitination of RPA194 and boosts the transcription activity of Pol I, promoting BC progression through increasing protein synthesis rates. a–e, g–i, Data shown as mean ± SEM. Statistical significance was calculated by two-tailed unpaired Student’s t-test. Source data are provided as a Source Data file.