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miR-1202通过向HMGCL来调节BPH-1细胞增殖,细胞亡和上皮细胞转变为介质细胞

Zhenting Wang, Xianlai Yin, Peng Yang

Acta biochimica et biophysica Sinica

|March 29, 2024

概括

微RNA-1202 (miR-1202) 在良性前列腺增生 (BPH) 中升高,通过向HMGCL,促进细胞生长和上皮细胞转化为介质细胞 (EMT). 这一途径涉及Wnt/β-catenin在BPH进展中的信号传递.

科学领域:

泌尿器科泌尿器科泌尿器科泌尿器科
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

良性前列腺增生 (BPH) 是一种常见的疾病,其特征是前列腺扩大和下泌尿道症状.
皮质到介质细胞过渡 (EMT) 和Wnt信号通路调节障碍与BPH病变有关.
微RNAs (miRNAs) 在调节基因表达方面发挥着至关重要的作用,并且在疾病发展中越来越被认可.

研究的目的:

研究miR-1202在良性前列腺增生 (BPH) 中的作用.
阐明miR-1202影响BPH细胞表型的分子机制,包括EMT和Wnt/β-catenin信号传递.
为了确定参与BPH病理的miR-1202的下游目标.

主要方法:

在人类BPH样本中分析miR-1202表达.
在体外研究中,使用用TGF-β治疗的BPH-1细胞来评估miR-1202过度表达和抑制对细胞存活,细胞亡和EMT标记物的影响.
对Wnt/β-catenin信号通路激活的研究.
路西法酶记者分析证实了miR-1202.2对HMGCL的直接向.
对HMGCL的过度表达研究,以评估其功能作用.
在BPH的老鼠模型中的体内验证.

主要成果:

在BPH组织和细胞中,miR-1202的表达显著上调.
过度表达miR-1202促进BPH-1细胞增殖,DNA合成和生存,同时抑制细胞亡.
miR-1202通过降低E-cadherin和增加维门丁,N-cadherin和牛表达来诱导EMT.
miR-1202增强了Wnt/β-catenin通路的活性,增加了Wnt1,c-Myc和cyclin D1.1的水平.
HMGCL被确定为miR-1202的直接标,miR-1202抑制了HMGCL的表达.
过度表达HMGCL可以抵消miR-1202的亲BPH效应,包括细胞增殖,细胞亡,EMT和Wnt信号传递.
在体内,BPH模型显示Ki67和维丁升高,E-cadherin和HMGCL降低.

结论:

miR-1202是良性前列腺增生症中关键的致癌性miRNA.
miR-1202通过增强细胞增殖,抑制细胞亡,并通过向HMGCL驱动EMT来促进BPH进展.
Wnt/β-catenin通路参与了miR-1202/HMGCL轴介导的BPH表型调节.

关键词:

3-基-3-甲基氨基-CoA溶解酶 (HMGCL) 是一种在Wnt/β-catenin路径中.良性前列腺增生症 (BPH) 是一种皮质转化为介质细胞的过渡 (EMT)这里是 miR-1202 的位置.

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