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Song, Mei; Yeku, Oladapo O; Rafiq, Sarwish; Purdon, Terence; Dong, Xue; Zhu, Lijing; Zhang, Tuo; Wang, Huan; Yu, Ziqi; Mai, Junhua; Shen, Haifa; Nixon, Briana; Li, Ming; Brentjens, Renier J; Ma, Xiaojing
Nature communications, 12/2020, Volume: 11, Issue: 1Journal Article
Immunosuppressive tumor microenvironment (TME) and ascites-derived spheroids in ovarian cancer (OC) facilitate tumor growth and progression, and also pose major obstacles for cancer therapy. The molecular pathways involved in the OC-TME interactions, how the crosstalk impinges on OC aggression and chemoresistance are not well-characterized. Here, we demonstrate that tumor-derived UBR5, an E3 ligase overexpressed in human OC associated with poor prognosis, is essential for OC progression principally by promoting tumor-associated macrophage recruitment and activation via key chemokines and cytokines. UBR5 is also required to sustain cell-intrinsic β-catenin-mediated signaling to promote cellular adhesion/colonization and organoid formation by controlling the p53 protein level. OC-specific targeting of UBR5 strongly augments the survival benefit of conventional chemotherapy and immunotherapies. This work provides mechanistic insights into the novel oncogene-like functions of UBR5 in regulating the OC-TME crosstalk and suggests that UBR5 is a potential therapeutic target in OC treatment for modulating the TME and cancer stemness.
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