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USP39/SMC4促进肝瘤细胞增殖和5-FU抗性

Bo Zhou¹, Jie Li¹, Shuai Wu¹

¹Department of Hepatobiliary Surgery, Daping Hospital, Army Medical University, No. 10, Changjiang Road, Daping, Yuzhong District, Chongqing, 400042, China.

Scientific reports

|March 15, 2025

概括

在肝细胞癌 (HCC) 的发展和进展中,对4号染色体 (SMC4) 和全素特异性酶39 (USP39) 的结构维护至关重要. 准SMC4,USP39,TIAL1或ZNF207可以克服HC的耐药性.

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:

肝细胞癌 (HCC) 由于高死亡率和不良预后,对全球健康构成重大挑战.
第4染色体结构维护 (SMC4) 的过度表达与包括HCC在内的各种癌症有关,与晚期瘤阶段和低生存率相关.
乌比基特异性酶39 (USP39) 在HCC病变发生中的作用及其与SMC4的相互作用需要进一步阐明.

研究的目的:

研究USP39和SMC4在肝细胞癌的发展和进展中的作用.
探索针对USP39/SMC4轴的潜力,以克服HCC的耐药性.
为了确定SMC4的潜在下游目标,参与HCC扩散和耐药性.

主要方法:

生物信息学分析以将SMC4表达与临床参数相关联,并确定潜在的相互作用蛋白质.
定量实时PCR (qPCR),西部涂抹和免疫组织化学 (IHC) 来评估USP39和SMC4在HCC组织和细胞系中的表达.
在体外测试 (MTT,EDU,伤口愈合) 评估USP39/SMC4在细胞活力,增殖和迁移中的功能作用,并评估基因淘汰后的药物敏感性.

主要成果:

在HCC组织和肝瘤细胞中观察到USP39和SMC4的高表达,与TNM阶段和不良预后有显著的相关性.
发现USP39/SMC4轴增强肝细胞癌细胞活力和增殖.
击败SMC4,TIAL1或ZNF207恢复了耐药HCC细胞对5-甲 (5-FU) 的敏感性,抑制了活力和增殖.

结论:

USP39/SMC4通路在HCC进展中发挥着关键作用,并有助于化学抵抗.
SMC4可能会调节HCC的耐药性,可能通过与TIAL1和ZNF207.7的相互作用.
向SMC4,USP39,TIAL1或ZNF207代表了克服肝细胞癌中耐药性的潜在治疗策略.

关键词:

药物耐药性药物耐药性药物耐药性肝细胞癌是肝细胞癌.核武器的扩散在SMC4中,SMC4是SMC4.USP39 美国39

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