EPISODE · Dec 9, 2025 · 19 MIN
306-NSD2与去势抵抗性前列腺癌谱系重塑
from 聊聊Sci
本研究探讨了去势抵抗性前列腺癌 (CRPC) 产生耐药性的机制，尤其关注其向高侵袭性的神经内分泌亚型（CRPC-NE）演变的路线。通过对小鼠和人类类器官模型进行分析，研究人员发现组蛋白甲基转移酶 NSD2 是驱动谱系可塑性并维持这种耐药神经内分泌状态的关键因子。在机制上，NSD2通过调控 H3K36me2 组蛋白标记来维持抗性，高 NSD2 表达与患者较差的总生存率显著相关。重要发现是，基因靶向或药物抑制 NSD2 能够逆转神经内分泌表型，促使细胞重新表达雄激素受体（AR）。这种逆转有效地 恢复了 CRPC 细胞对雄激素受体抑制剂恩杂鲁胺的敏感性，为治疗晚期前列腺癌提供了联合抑制 NSD2 和 AR 通路的临床前依据。References: Li J J, Vasciaveo A, Karagiannis D, et al. NSD2 targeting reverses plasticity and drug resistance in prostate cancer[J]. Nature, 2025: 1-11.前往小宇宙评论区与主播互动
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306-NSD2与去势抵抗性前列腺癌谱系重塑
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