Cancer Cell：科学家发现促进前列腺癌的新致癌转录因子

2016-06-04 佚名生物谷

本文亮点： TRIM24在SPOP突变前列腺癌和去势抵抗性前列腺癌（CRPC）中介导肿瘤细胞增殖 TRIM24在CRPC中与雄激素受体（AR）共同激活促增殖基因 TRIM24蛋白在CRPC中存在增加的情况并可以预测疾病复发 TRIM24的bromodomain介导CRPC生长，是一个潜在的药物靶点近日来自哈佛大学医学院的研究人员在国际学术期刊Cancer Cell上发表了一项最新研

本文亮点：

TRIM24在SPOP突变前列腺癌和去势抵抗性前列腺癌（CRPC）中介导肿瘤细胞增殖

TRIM24在CRPC中与雄激素受体（AR）共同激活促增殖基因

TRIM24蛋白在CRPC中存在增加的情况并可以预测疾病复发

TRIM24的bromodomain介导CRPC生长，是一个潜在的药物靶点

近日来自哈佛大学医学院的研究人员在国际学术期刊Cancer Cell上发表了一项最新研究进展，他们在SPOP突变前列腺癌以及去势抵抗型前列腺癌中发现了促进癌细胞增殖的关键分子，为这两种前列腺癌的治疗提供了新靶点。

雄激素受体（AR）信号是导致前列腺癌发生的关键驱动因素，虽然对于晚期患者来说去势治疗在短时间内比较有效，但是经常出现肿瘤复发形成去势抵抗型前列腺癌，而这种癌症通常都是致命的。

在这项研究中，研究人员发现在前列腺癌中一种叫做SPOP（speckle-type POZ protein）的蛋白经常发生促癌突变，这种突变蛋白能够通过稳定在低雄激素水平状态下具有促增殖作用的TRIM24蛋白导致癌症的进一步发展。TRIM24能够增强AR信号，而AR和TRIM24会共同激活在CRPC中存在显著上调的基因。

研究人员发现从原发性前列腺癌变成去势抵抗型前列腺癌的过程中，TRIM24的蛋白表达水平会发生增加，并且TRIM24的蛋白水平以及AR/TRIM24相关的基因标记都能够预测疾病的复发。

通过对CRPC细胞进行分析，研究人员发现TRIM24的bromodomain以及AR-interacting motif在促进细胞增殖的作用中非常关键，因此靶向TRIM24的bromodomain或可成为开发SPOP突变型前列腺癌以及CRPC治疗药物的新策略。

原始出处

Anna C. Groner, Laura Cato, Jonas de Tribolet-Hardy, Tiziano Bernasocchi.TRIM24 Is an Oncogenic Transcriptional Activator in Prostate Cancer.Cancer Cell.2016

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2017-02-26 mjldent

#转录#

73 0
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2016-11-17 维他命

#CEL#

65 0
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2017-01-31 zhaozhouchifen

#Cell#

70 0
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2016-11-25 12498e67m28暂无昵称

#cancer cell#

67 0
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2016-11-27 旅苦化文_208

#科学家发现#

57 0
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2016-06-06 jambiya

#致癌#

58 0
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2016-06-06 lanyan20020090

#转录因子#

62 0
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2016-06-05 沉心多思

不错的文章，多学习

136 0
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2016-06-05 沉心多思

不错的文章，多学习

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