甲状腺乳突癌
基因沉默
甲状腺癌
癌症研究
甲状腺癌
小RNA
癌变
细胞生长
癌症
活力测定
免疫印迹
医学
细胞
内科学
生物
甲状腺
基因
生物化学
作者
Tianbin Huang,Shanbin Guan,Changquan Wang
出处
期刊:PubMed
日期:2022-05-01
卷期号:52 (3): 426-438
被引量:2
摘要
The purpose of this study was to explore the function and mechanism of LncRNA CERS6-AS1 on papillary thyroid cancer.CERS6-AS1, miR-497-5p, and LASP1 expression in papillary thyroid cancer tissues and cells were detected by RT-PCR. The relationship between CERS6-AS1 expression and clinical characteristics was analyzed, and overall survival was evaluated via Kaplan-Meier analysis. Cell activity was tested by cell counting kit-8, cell reactive oxygen species was detected by DCFH-DA method, and cell iron ion was detected by iron analysis kit. The relationship among CERS6-AS1, miR-497-5p, and LASP1 was confirmed by luciferase reporter gene detection, RNA pull-down detection, and RIP detection. The expression of related proteins was assessed by western blot or immunohistochemistry.High level of CERS6-AS1 and LASP1 was detected in papillary thyroid cancer tissues and cells and predicted poor prognosis. In contrast, miR-497-5p was decreased in papillary thyroid cancer tissues and cells, which was positively correlated with prognosis. Silencing CERS6-AS1 suppressed cell viability and increased ferroptosis in papillary thyroid cancer. LASP1 was modulated by CERS6-AS1 through sponging miR-497-5p. Up-regulation of LASP1 or silencing miR-497-5p could weaken the effect of CERS6-AS1 on papillary thyroid cancer cells. Silencing CERS6-AS1 restrained the growth of xenografted tumors.Our findings demonstrated that down-regulation of CERS6-AS1 reduced cell viability and amplified cell ferroptosis by modulating the miR-497-5p/LASP1 axis in papillary thyroid cancer.
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