南美超级胎牛血清999尝鲜特惠
转染试剂低至5折
基质胶阶梯特惠
积分商城,好礼送不停
南美超级胎牛血清999尝鲜特惠
转染试剂低至5折
基质胶阶梯特惠
积分商城,好礼送不停
分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

lncRNA SNHG3作为新型抑癌基因通过AKT/mTOR/ERK通路调控甲状腺乳头状癌增殖和转移

lncRNA SNHG3 acts as a novel Tumor Suppressor and regulates Tumor Proliferation and Metastasis via AKT/mTOR/ERK pathway in Papillary Thyroid Carcinoma

Yu Duan, Zhiyong Wang, Lijuan Xu, Li Sun, Hairong Song, Huiqing Yin, Fucheng He

Journal:Journal of Cancer

IF:3.57

DOI:10.7150/jca.42070

PMID:32284745

Published:2020-03-15

research field:免疫学呼吸生物学生物化学

Abstract

The incidence of papillary thyroid carcinoma (PTC) has been increased rapidly in recent decades. Long noncoding RNAs (lncRNA) are a class of non-protein-coding transcripts and play critical roles in regulating gene expression and influence biological behaviors of multiple cancers, including PTC. Here, we discovered that lncRNA SNHG3 was significantly downregulated in PTC tissues and cell lines, the expression of SNHG3 was negatively correlated with the TNM stage and poor prognosis of PTC patients. Functional studies illustrated that the depletion of SNHG3 via CRISPR/Cas9 technology promoted the proliferation, migration and invasion abilities of PTC cells. Tumor xenograft models confirmed the tumor-promoting role of silenced SNHG3 in vivo . Further mechanistic analyses revealed that knockout of SNHG3 activated the AKT/mTOR/ERK pathway in PTC cell lines and the mTOR inhibitor AZD8055 abrogated the tumor-promoting effect induced by SNHG3 inhibition. Taken together, our findings identified a lncRNA SNHG3 that functions its tumor-suppressor role during PTC development and SNHG3 might serve as a promising candidate for target therapy of PTC.

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