在促进前列腺瘤发生方面,NSD2是AR/FOXA1新增强酶体的必需子单元
Abhijit Parolia1,2,3,4, Sanjana Eyunni1,2,5,6, Brijesh Kumar Verma7,6
1Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.
bioRxiv : the preprint server for biology
|March 11, 2024
概括
核受体结合SET域蛋白2 (NSD2) 通过重新编程雄激素受体 (AR) 结合,驱动前列腺癌的进展. 抑制NSD2及其对应物NSD1显示出治疗晚期前列腺癌的前景.
科学领域:
- 分子生物学分子生物学
- 癌症生物学 癌症生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
背景情况:
- 雄激素受体 (AR) 调节正常的前列腺细胞分化,但在前列腺瘤中被重新编程以驱动癌症表型.
- 在癌症中AR重编程背后的分子机制仍然不太清楚.
结论:
- NSD2是AR"新增强酶体"的关键组成部分,驱动前列腺癌基因表达.
- NSD1和NSD2是治疗晚期前列腺癌和其他恶性瘤的可行的共同标.
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