Oncogene:BMI1直接受雄激素受体调控来促进前列腺癌的去势抵抗性

2019-09-12 AlexYang MedSci原创

B淋巴瘤Mo-MLV插入区1(BMI1)已经报道为是一个致瘤蛋白。BMI1抑制肿瘤抑制因子来促进细胞的增殖、上皮-间质转化(EMT)和癌症进展。尽管已知BMI1在许多癌症类型中均表达增加,BMI1上调的机制仍旧不清楚。最近,有研究人员对3组前列腺癌(PCa)基因组数据进行了整体的分析,并发现BMI和雄激素受体(AR)具有正相关关系,表明了AR可能对BMI1具有调控作用。之后,研究人员展示了二氢睾酮

B淋巴瘤Mo-MLV插入区1(BMI1)已经报道为是一个致瘤蛋白。BMI1抑制肿瘤抑制因子来促进细胞的增殖、上皮-间质转化(EMT)和癌症进展。尽管已知BMI1在许多癌症类型中均表达增加,BMI1上调的机制仍旧不清楚。

最近,有研究人员对3组前列腺癌(PCa)基因组数据进行了整体的分析,并发现BMI和雄激素受体(AR)具有正相关关系,表明了AR可能对BMI1具有调控作用。之后,研究人员展示了二氢睾酮(DHT)能够同时上调BMI1的mRNA和蛋白水平,且BMI1在去势抵抗性前列腺癌(CRPC)人类患者和小鼠异种种植模型中均增加。研究人员进一步鉴定了AR在BMI1启动子/增强子上的结合位点,并利用基因编辑技术确定了BMI1是AR的直接靶基因。另外,他们还阐释了BMI1的高表达对去势抵抗性是非常重要的。

最后,研究人员指出,BMI1特异性抑制剂可以作为CRPC的有效治疗方法。

原始出处:


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    2020-04-29 cy0324
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    2020-03-28 yige2012
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    2019-09-14 zsyan
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    2019-09-13 深海的鱼

    学习学习学习

    0

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    2019-09-12 misszhang

    前列腺癌相关研究,学习了,谢谢梅斯

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