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DTX3L and ARTD9 inhibit IRF1 expression and mediate in cooperation with ARTD8 survival and proliferation of metastatic prostate cancer cells

机译:DTX3L和ARTD9抑制IRF1表达并与ARTD8协同介导转移性前列腺癌细胞的存活和增殖

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摘要

BackgroundProstate cancer (PCa) is one of the leading causes of cancer-related mortality and morbidity in the aging male population and represents the most frequently diagnosed malignancy in men around the world. The Deltex (DTX)-3-like E3 ubiquitin ligase (DTX3L), also known as B-lymphoma and BAL-associated protein (BBAP), was originally identified as a binding partner of the diphtheria-toxin-like macrodomain containing ADP-ribosyltransferase-9 (ARTD9), also known as BAL1 and PARP9. We have previously demonstrated that ARTD9 acts as a novel oncogenic survival factor in high-risk, chemo-resistant, diffuse large B cell lymphoma (DLBCL). The mono-ADP-ribosyltransferase ARTD8, also known as PARP14 functions as a STAT6-specific co-regulator of IL4-mediated proliferation and survival in B cells.
机译:背景技术前列腺癌(PCa)是男性老龄化人群中与癌症相关的死亡率和发病率的主要原因之一,代表着全世界男性最常被诊断出的恶性肿瘤。 Deltex(DTX)-3-like E3泛素连接酶(DTX3L),也称为B淋巴瘤和BAL相关蛋白(BBAP),最初被确定为含有ADP-核糖基转移酶的白喉毒素样大域的结合伴侣。 -9(ARTD9),也称为BAL1和PARP9。我们以前已经证明ARTD9在高风险,耐化学性,弥漫性大B细胞淋巴瘤(DLBCL)中充当新型致癌生存因子。单-ADP-核糖基转移酶ARTD8,也称为PARP14,充当IL4介导的B细胞增殖和存活的STAT6特异性协同调节剂。

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