西斯特
基因敲除
基因沉默
长非编码RNA
小干扰RNA
细胞生长
生物
癌症研究
分子生物学
转染
细胞
下调和上调
细胞培养
X-失活
基因
生物化学
遗传学
X染色体
作者
Yongming Liu,Yuan Zhang,Jinxue Zhang,Jingchang Ma,Xuexue Xu,Yuling Wang,Ziqing Zhou,Dongxu Jiang,Shen Shen,Yong Ding,Yong Zhou,Ran Zhuang
标识
DOI:10.3389/fonc.2021.601982
摘要
Osteosarcoma (OS) is a highly malignant and aggressive bone tumor. This study was performed to explore the mechanisms of HuR (human antigen R) in the progression of OS.HuR expression levels in OS tissues and cells were detected by immunohistochemistry and western blotting. HuR siRNA was transfected into SJSA-1 OS cells to downregulate HuR expression, and then cell proliferation, migration, and epithelial-mesenchymal transition (EMT) were evaluated. RNA immunoprecipitation was performed to determine the association of the long non-coding RNA (lncRNA) XIST and argonaute RISC catalytic component (AGO) 2 with HuR. Fluorescence in situ hybridization analysis was performed to detect the expression of lncRNA XIST. Western blotting and immunofluorescence assays were performed to observe AGO2 expression after HuR or/and lncRNA XIST knockdown.Knockdown of HuR repressed OS cell migration and EMT. AGO2 was identified as a target of HuR and silencing of HuR decreased AGO2 expression. The lncRNA XIST was associated with HuR-mediated AGO2 suppression. Moreover, knockdown of AGO2 significantly inhibited cell proliferation, migration, and EMT in OS.Our findings indicate that HuR knockdown suppresses OS cell EMT by regulating lncRNA XIST/AGO2 signaling.
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