Yasheng Zhu

TL;DR: It is shown that PD-L1 protein abundance is regulated by cyclin D–CDK4 and the cullin 3–SPOP E3 ligase via proteasome-mediated degradation, which reveals the potential for using combination treatment with CDK4/6 inhibitors and PD-1–PD-L 1 immune checkpoint blockade to enhance therapeutic efficacy for human cancers.

TL;DR: It is demonstrated that wild-type SPOP binds to and induces ubiquitination and proteasomal degradation of BET proteins by recognizing a degron motif common among them, and resistance to BET inhibitors in SPOP-mutant prostate cancer can be overcome by combination with AKT inhibitors.

TL;DR: The results demonstrate that urine MALAT-1 is a promising biomarker for predicting prostate cancer risk, and as an independent predictor of PCa, the MALat-1 score was significantly higher in men with a positive biopsy than in those with a negative biopsy.

TL;DR: In this paper, the authors have profiled the transcriptomes of 36,424 single cells from 13 prostate tumours and identified the epithelial cells underlying disease aggressiveness. But the transcriptomic heterogeneity of prostate cancer is poorly understood.

TL;DR: This work demonstrates that SPOP, functioning as an E3 ubiquitin ligase substrate-binding protein, promotes ubiquitination and proteasome degradation of wild-type ERG by recognizing a degron motif at the N terminus of ERG and suggests that overcoming ERG resistance to SPOP-mediated degradation represents a viable strategy for treatment of prostate cancer.