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克洛法齐明治疗调节关键的非编码RNA,与致死性前列腺癌的瘤进展和抗药性有关

Sarah Batten¹, Harish Kumar^1,2, Jeremiah Pfitzer¹

¹Department of Drug Discovery & Development, Harrison College of Pharmacy, Auburn University, Auburn, AL 36849, USA.

International journal of molecular sciences

|November 27, 2025

概括

克洛法齐明 (CLF) 通过减少癌细胞迁移和干细胞,在治疗晚期前列腺癌 (PCa) 中表现有前途. 这种FDA批准的药物单独或与纳税化合物一起有效,为转移性割耐药PCa提供了新的治疗途径.

科学领域:

在瘤学瘤学.
药理学药理学是指药理学的学科.
癌症生物学癌症生物学

背景情况:

转移性割耐药前列腺癌 (mCRPC) 带来了重大的临床挑战,包括增加的攻击性和对标准疗法的耐药性.
癌症干细胞 (CSC) 和上皮转化为介质细胞的转变 (EMT) 有助于mCRPC的进展和治疗耐药性.
克洛法齐明 (CLF) 是FDA批准的治疗麻风的药物,已在其他血液性恶性瘤中证明有效.

研究的目的:

为了评估Clofazimine (CLF) 作为单一药物的有效性,以及与多种mCRPC患者细胞系治疗的纳税剂的组合.
研究CLF对前列腺癌细胞迁移,干细胞 (ALDH活性) 和上皮细胞转移到介质细胞 (EMT) 的影响.
阐明CLF在mCRPC中的抗癌作用背后的分子机制.

主要方法:

利用了一个代表患者多样性的mCRPC细胞系的面板.
采用微流体测试来评估癌细胞迁移和转移潜力.
测量了作为癌症干细胞 (CSC) 标记物的化脱酶 (ALDH) 活性.
进行了批量和单细胞RNA测序 (RNAseq),功能验证和分析.

主要成果:

单独使用CLF和与纳税素结合使用,对抗mCRPC细胞系的疗效得到了证明.
癌细胞转移显著减少癌细胞迁移和转移潜力.
结核细胞降低了ALDH活性,表明癌症干细胞 (CSCs) 的减少.
RNAseq分析显示,CLF诱导了亡,ER压力和线粒体功能障碍,同时调节了MALAT1和NEAT1等非编码RNA.

结论:

克洛法齐明 (CLF) 是一种强效的治疗药物,可单独或与税结合,对抗转移性割抵抗性前列腺癌 (mCRPC).
CLF针对mCRPC进展的关键驱动因素,包括癌细胞迁移,干细胞和EMT.
分子机制包括亡诱导,ER压力,线粒体功能障碍和关键非编码RNA的调制,突出显示了CLF在克服药物耐药性的潜力.

关键词:

在RNAseqqq中使用.克洛法齐米因 (Clofazimine) 是一种类药物.组合疗法治疗组合治疗.在ncRNA中,我们可以 mCRPC 的使用情况.没有编码的RNA.标杆菌的耐药性标杆菌的耐药性

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