长非编码RNA PTCSC3通过降低长非编码RNA MIR100HG 的调节来抑制三阴性乳腺癌
Guojun Zhang1, Lei Gao1, Junliang Zhang1
1Department of General Surgery, Changle People's Hospital, Changle County, Shandong 262499, P.R. China.
Oncology letters
|July 7, 2023
概括
长非编码RNA (lncRNA) PTCSC3在三阴性乳腺癌 (TNBC) 中充当瘤抑制剂. 它抑制癌细胞活力,通过降低MIR100HG的调节促进细胞亡,影响患者的存活率.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 长非编码RNA (lncRNA) PTCSC3是甲状腺癌和质瘤中已知的瘤抑制剂.
- 它在三阴性乳腺癌 (TNBC) 中的作用仍然在很大程度上未被探索.
研究的目的:
- 研究PTCSC3在三阴性乳腺癌 (TNBC) 的功能和分子机制.
- 探索PTCSC3,MIR100HG和TNBC进展之间的关系.
主要方法:
- 在82个TNBC患者组织中分析PTCSC3和MIR100HG表达.
- 细胞活力 (CCK-8) 和细胞亡 (Annexin V-FITC) 的测定.
- 西方斑点分析用于调查信号通路 (河马通路).
主要成果:
- 在TNBC组织中,PTCSC3的下调,MIR100HG的上调.
- 低的PTCSC3和高的MIR100HG表达与患者的生存率差相关.
- 过度表达PTCSC3抑制了MIR100HG,抑制了TNBC细胞活力,并通过Hippo通路促进了细胞亡.
- 过度表达MIR100HG促进了TNBC细胞活力和抑制了细胞亡,抵消了PTCSC3的影响.
结论:
- lncRNA PTCSC3通过降低MIR100HG的调节,在TNBC中起到瘤抑制作用.
- PTCSC3 抑制了 TNBC 细胞活力,并促进了细胞亡,可能通过河马信号通路.
- PTCSC3和MIR100HG是TNBC患者显著的预后生物标志物.
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