在S100A4调节细胞增殖,细胞亡和纤维化在前列腺增生
Liang Yang1, Jiang Liu1, Jing Yin2
1Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
The international journal of biochemistry & cell biology
|February 15, 2024
概括
S100结合蛋白A4 (S100A4) 在良性前列腺增生 (BPH) 的发展中起着关键作用. 向S100A4可能为治疗BPH及其相关下尿路症状 (LUTS) 提供一种新的治疗策略.
科学领域:
- 泌尿器科 泌尿器科 泌尿器科 泌尿器科
- 细胞生物学 细胞生物学
- 分子医学是分子医学.
背景情况:
- 良性前列腺增生症 (BPH) 是老年男性中普遍存在的疾病,导致下泌尿道症状 (LUTS).
- 导致BPH发病的精确分子机制尚不完全理解.
- S100结合蛋白A4 (S100A4) 与疾病相关的细胞过程有关,包括增殖和亡.
研究的目的:
- 研究S100结合蛋白A4 (S100A4) 在良性前列腺增生 (BPH) 的发展中的作用.
- 阐明通过S100A4影响前列腺组织的信号通路.
主要方法:
- 利用人类前列腺细胞系,初级老鼠细胞,人类组织,并建立了BPH老鼠模型.
- 通过使用qRT-PCR,免疫光,西部斑点和免疫组织化学来评估S100A4表达和局部化.
- 创建了S100A4倒置/过度表达模型,并用S100A4抑制剂尼克洛萨米德治疗BPH大鼠.
主要成果:
- 在BPH组织中S100A4表达升高,并局部化到前列腺层和上皮.
- S100A4 knockdown诱导了亡,抑制了增殖,并减少了纤维化标志物.
- S100A4过度表达逆转了这些效应,影响了ERK和Wnt/β-catenin通路.
结论:
- S100结合蛋白A4 (S100A4) 显著促进良性前列腺增生 (BPH) 的发展.
- 通过ERK和Wnt/β-catenin信号传递,S100A4调节细胞增殖,细胞亡和纤维化.
- S100A4代表了BPH的一个潜在的新疗法标.
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