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长非编码RNACCAT2的破坏抑制了人类喉状细胞癌的恶性表型

M Li¹, J An², H Ren³

¹Department of Otolaryngology-Head and Neck Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

Bulletin of experimental biology and medicine

|October 24, 2023

概括

结肠癌相关的转录2 (CCAT2),一个长的非编码RNA,在喉状细胞癌 (LSCC) 中高度表达. 沉默CCAT2抑制LSCC细胞的增殖和入侵,这表明它是一个治疗目标.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
遗传学遗传学是一个

背景情况:

喉平细胞癌 (LSCC) 是一个重大的健康问题.
长非编码RNAs (lncRNAs) 在LSCC病变发生中的作用越来越被认可.
结肠癌相关转录2 (CCAT2) 是一种涉及各种癌症的lncRNA.

研究的目的:

研究人类LSCC中CCAT2的生物学作用和潜在机制.
为了确定CCAT2表达和LSCC患者预后之间的相关性.
评估CCAT2作为LSCC的潜在治疗标和预后生物标志物.

主要方法:

定量实时PCR测量LSCC组织和细胞系中的CCAT2表达.
细胞计数套件-8,Transwell测定和流动细胞计量以评估细胞增殖,入侵和细胞亡.
在裸体小鼠体内LSCC异种移植模型以评估瘤生长.
西方涂抹和免疫组织化学检测蛋白表达 (β-catenin,CDK8).

主要成果:

与正常对照组相比,LSCC组织和细胞中CCCAT2表达显著增加.
高CCAT2表达与LSCC患者5年整体存活率较差相关.
CCAT2的淘汰抑制了LSCC细胞的增殖和入侵,同时促进了细胞亡.
在体内,CCAT2倒置抑制了瘤的生长,体积和体重.
CCAT2抑制下调β-catenin和CDK8的表达,抑制Wnt/β-catenin信号通路.

结论:

通过增强扩散和入侵,CCAT2在促进LSCC进展方面发挥着至关重要的作用.
CCAT2至少部分通过调节Wnt/β-catenin信号通路而起作用.
CCAT2是LSCC的潜在预后生物标志物和治疗点.

关键词:

灭症 (apoptosis) 是一种死亡的过程.循环林依赖性激酶8的作用喉皮状细胞癌瘤长非编码RNA结肠癌相关的转录2 (CCAT2)它们的扩散和扩散.

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