简基因促进了抵抗割的前列腺癌的进展
Yigeng Feng1, Hongwen Cao1, Dan Wang1
1Surgical Department I (Urology Department), LONGHUA Hospital Shanghai University of Traditional Chinese Medicine, Xuhui District, Shanghai 200032, China.
Acta biochimica Polonica
|December 15, 2023
概括
过度表达C-Jun N-终端激酶 (JNK) 通过增强细胞活力和入侵,加速割抵抗性前列腺癌 (CRPC) 的进展. 较低的JNK表达与CRPC患者更好的生存率相关.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
背景情况:
- 前列腺癌是全球男性普遍存在的恶性瘤.
- 抗割前列腺癌 (CRPC) 是一个重大的临床挑战.
- 了解CRPC进展的分子驱动因素对于治疗开发至关重要.
研究的目的:
- 调查c-Jun N-终端激酶 (JNK) 在抵抗割的前列腺癌 (CRPC) 的进展中的作用.
- 在CRPC患者中确定JNK表达水平和临床参数之间的关系.
主要方法:
- 已确立的JNK过度表达和淘汰PC-3前列腺癌细胞系.
- 使用定量PCR (qPCR) 和西式涂抹来评估基因和蛋白质表达.
- 进行了MTT和Matrigel入侵试验,以评估细胞活力和侵入性.
- 采用卡普兰-梅尔分析来估计生存率和皮尔森的相关性,用于JNK和前列腺特异性抗原 (PSA) 的关系.
主要成果:
- 在CRPC组织中JNK表达的升高与更高的格莱森得分和PSA值相关.
- 卡普兰-梅尔分析表明,低JNK表达与改善的整体和第二次无进展生存率有关.
- 在体外研究表明,JNK过度表达增加了PC-3细胞活力,细胞外信号调节激酶 (ERK) 和矩阵金属蛋白酶1 (MMP1) 的侵入和表达.
结论:
- 过度表达JNK显著促进CRPC的进展.
- 通过对ERK和MMP1.1进行升级监管,JNK促进CRPC的发展.
- 准JNK可能是CRPC的潜在治疗策略.
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