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前列腺癌的骨转移进展受TRIM28-LDHA介导的新陈代谢的调节

Miyeong Kim¹, Han Cong¹, Ryan Goettl¹

¹University of Kentucky, Lexington, KY, United States.

Molecular cancer research : MCR

|October 17, 2025

概括

酸化TRIM28 (也称为KAP1) 通过上调乳酸脱酶A (LDHA) 和糖解,驱动骨前列腺癌的进展. 用LDH抑制剂向TRIM28-LDHA轴可能可以缓解晚期前列腺癌.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
生物化学生物化学

背景情况:

抗割前列腺癌 (CRPC) 是前列腺癌 (PCa) 的晚期阶段,通常导致致命的骨转移.
目前的雄激素受体 (AR) 抑制剂缺乏治愈疗效,突出显示了需要新的治疗策略.
TRIM28 (KAP1) 是由RSK1在S473酸化的转录因子,促进基因激活.

研究的目的:

研究TRIM28酸化在CRPC骨转移中的作用.
在骨转移PCa.中识别TRIM28调节的新型基因.
评估针对TRIM28-LDHA轴的治疗潜力.

主要方法:

生物信息和基因组分析以确定TRIM28诱导的基因.
在CRPC骨转移中检测TRIM28 S473酸化的西部涂抹.
在小鼠的骨注射模型中,以研究PCa进展.
乳酸脱酶 (LDH) 抑制剂疗效的评估.

主要成果:

在CRPC骨转移中检测到TRIM28 S473酸化,与激活的RSK激酶相关.
乳酸脱酶A (LDHA) 被确定为一种新的TRIM28诱导基因,以pS473-TRIM28依赖的方式调节.
TRIM28-LDHA轴促进糖解和乳酸生产,推动前列腺瘤在骨中的进展.
药理上抑制LDH活性减轻了骨中PCa的发展.

结论:

TRIM28-LDHA轴在前列腺癌骨转移的进展中发挥着至关重要的作用.
针对TRIM28介导的LDHA上调和随后的糖解,为高级PCa提供了潜在的治疗策略.
抑制LDH在缓解CRPC骨转移方面表现有前途.

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