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长非编码RNAEGOT与敏感性有关,通过准miR-641/PTEN轴,有助于甲状腺癌的进展

Ming Wang¹, Zhengchao Wei¹, Shuang Wang²

¹Department of Thyroid-Head and Neck Oncosurgery-1, Jilin Cancer Hospital, Changchun, Jilin Province, China.

|November 25, 2023

概括

长非编码RNA EGOT通过调节miR-641/PTEN通路来克服甲状腺癌中的放射性抗性. 这一发现为提高甲状腺癌治疗效率提供了潜在的新策略.

科学领域:

内分泌学在内分泌学.
在瘤学瘤学.
分子生物学分子生物学

背景情况:

甲状腺癌 (TC) 是全球常见的内分泌恶性瘤.
放射性 (¹³¹I) 治疗是TC的标准治疗方法,但耐药性限制了其临床疗效.
长非编码RNA (lncRNA) EGOT在TC细胞I抵抗中的作用尚不清楚.

研究的目的:

为了研究甲状腺癌细胞I抵抗中lncRNA EGOT的功能.
阐明EGOT在I抗性TC细胞中的作用的潜在分子机制.

主要方法:

建立了对抗I的TC细胞系.
对EGOT,PTEN和miR-641表达水平进行定量分析.
对EGOT对细胞活力,细胞亡和DNA损伤的影响的评估.
使用体外实验对EGOT/miR-641/PTEN监管轴的调查.

主要成果:

抗I的TC细胞表现出减少的EGOT和PTEN表达,以及增加的miR-641水平.
过度表达EGOT抑制了细胞活力,促进了细胞亡,并在耐药细胞中增强了DNA损伤.
通过向miR-641.1,发现EGOT可以通过向miR-641.1,提高PTEN表达的调节.
PTEN 枯竭或 miR-641 模仿转染逆转了 EGOT 对I 抵抗的有益影响.

结论:

lncRNA EGOT显著减弱了甲状腺癌细胞中的I电阻.
该机制涉及对miR-641/PTEN轴的EGOT定位.
EGOT有可能成为克服甲状腺癌中I电阻的治疗标,这需要进一步的临床验证.

关键词:

131I 阻力阻力阻力阻力在这里,我们可以使用PTEN.临床功能临床功能在cRNA EGOT中.在 miR-641 测试中,甲状腺癌是一种癌症.

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