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Long Noncoding RNA PVT1 Promotes Stemness and Temozolomide Resistance through miR-365/ELF4/SOX2 Axis in Glioma.
Experimental Neurobiology ( IF 2.4 ) Pub Date : 2021-7-8 , DOI: 10.5607/en20060
Rui Gong 1 , Zhi-Qiang Li 1 , Kai Fu 1 , Chao Ma 1 , Wei Wang 1 , Jin-Cao Chen 1
Affiliation  

Long non-coding RNA (lncRNA) are a class of non-coding RNAs demonstrated to play pivotal roles in regulating tumor progression. Therefore, deciphering the regulatory role of lncRNA in the development of glioma may offer a promising therapeutic target for treatment of glioma. We performed RT-qPCR analysis on the expression of lncRNA plasmacytoma variant translocation 1 (PVT1) and miR-365 in glioma tissues and cell lines. Cell proliferation and viability was assessed with CCK8 assay. Cell migration was assessed by wound healing assay. Transwell assay was used to assess cell invasion capacity. Expression of CD133+ cells was detected by flow cytometry. Western blot assay was used to detection the expression of ELF4 and stemness-related protein SOX2, Oct4 and Nanog. Bioinformatics and dual-luciferase assay were used to predict and validate the interaction between PVT1 and miR-365. Elevated PVT1 expression was observed in glioma tissues and cells. Knockdown of PVT1 and overexpression of miR-365 inhibited proliferation, migration, invasion and promoted stemness and Temozolomide (TMZ) resistance of glioma cells. PVT1 regulated ELF4 expression by competitively binds to miR-365. PVT1 regulated the stemness and sensitivity of TMZ of glioma cells through miR-365/ELF4/ SOX2 axis. This study identified that PVT1 promoted glioma stemness through miR-365/ELF4/SOX2 axis.

中文翻译:

长链非编码 RNA PVT1 通过胶质瘤中的 miR-365/ELF4/SOX2 轴促进干性和替莫唑胺抗性。

长链非编码 RNA (lncRNA) 是一类被证明在调节肿瘤进展中发挥关键作用的非编码 RNA。因此,破译lncRNA在胶质瘤发展中的调节作用可能为胶质瘤的治疗提供一个有希望的治疗靶点。我们对 lncRNA 浆细胞瘤变异易位 1 (PVT1) 和 miR-365 在胶质瘤组织和细胞系中的表达进行了 RT-qPCR 分析。用CCK8测定评估细胞增殖和活力。通过伤口愈合试验评估细胞迁移。Transwell测定用于评估细胞侵袭能力。通过流式细胞术检测CD133+细胞的表达。采用Western blot检测ELF4和干细胞相关蛋白SOX2、Oct4和Nanog的表达。生物信息学和双荧光素酶测定用于预测和验证 PVT1 和 miR-365 之间的相互作用。在胶质瘤组织和细胞中观察到 PVT1 表达升高。PVT1 的敲低和 miR-365 的过表达抑制了胶质瘤细胞的增殖、迁移、侵袭并促进了干细胞和替莫唑胺 (TMZ) 抗性。PVT1 通过与 miR-365 竞争性结合来调节 ELF4 的表达。PVT1通过miR-365/ELF4/SOX2轴调控胶质瘤细胞TMZ的干性和敏感性。该研究确定 PVT1 通过 miR-365/ELF4/SOX2 轴促进胶质瘤干细胞。侵袭并促进胶质瘤细胞的干性和替莫唑胺(TMZ)抗性。PVT1 通过与 miR-365 竞争性结合来调节 ELF4 的表达。PVT1通过miR-365/ELF4/SOX2轴调控胶质瘤细胞TMZ的干性和敏感性。该研究确定 PVT1 通过 miR-365/ELF4/SOX2 轴促进胶质瘤干细胞。侵袭并促进胶质瘤细胞的干性和替莫唑胺(TMZ)抗性。PVT1 通过与 miR-365 竞争性结合来调节 ELF4 的表达。PVT1通过miR-365/ELF4/SOX2轴调控胶质瘤细胞TMZ的干性和敏感性。该研究确定 PVT1 通过 miR-365/ELF4/SOX2 轴促进胶质瘤干细胞。
更新日期:2021-07-09
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