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Tumor Microenvironment: A Metabolic Player that Shapes the Immune Response.肿瘤微环境:塑造免疫反应的代谢参与者。
Int J Mol Sci. 2019 Dec 25;21(1):157. doi: 10.3390/ijms21010157.
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Long noncoding RNA ZFAS1 promotes tumorigenesis and metastasis in nasopharyngeal carcinoma by sponging miR-892b to up-regulate LPAR1 expression.长链非编码 RNA ZFAS1 通过海绵吸附 miR-892b 来上调 LPAR1 表达,促进鼻咽癌的发生和转移。
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Exosomal lncRNA ZFAS1 regulates esophageal squamous cell carcinoma cell proliferation, invasion, migration and apoptosis via microRNA-124/STAT3 axis.外泌体长链非编码 RNA ZFAS1 通过 microRNA-124/STAT3 轴调控食管鳞癌细胞的增殖、侵袭、迁移和凋亡。
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LncRNA MINCR regulates irradiation resistance in nasopharyngeal carcinoma cells via the microRNA-223/ZEB1 axis.长链非编码 RNA MINCR 通过 microRNA-223/ZEB1 轴调节鼻咽癌细胞的辐射抗性。
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Circular RNA CDR1as sponges miR-7-5p to enhance E2F3 stability and promote the growth of nasopharyngeal carcinoma.环状RNA CDR1as通过吸附miR-7-5p增强E2F3稳定性并促进鼻咽癌生长。
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长链非编码 RNA ZFAS1 通过海绵吸附 hsa-miR-7-5p 来上调 ENO2 从而促进鼻咽癌细胞的放射抵抗。

IncRNA ZFAS1 contributes to the radioresistance of nasopharyngeal carcinoma cells by sponging hsa-miR-7-5p to upregulate ENO2.

机构信息

Department of Otolaryngology, Head and Neck Surgery, West China Hospital, Sichuan University , Sichuan, China.

出版信息

Cell Cycle. 2021 Jan;20(1):126-141. doi: 10.1080/15384101.2020.1864128. Epub 2020 Dec 20.

DOI:10.1080/15384101.2020.1864128
PMID:33342344
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7849681/
Abstract

Previous research revealed that lncRNA ZFAS1 could promote nasopharyngeal carcinoma (NPC) by inhibiting its downstream target axis. However, the association between ZFAS1 and radioresistant NPC cells is unclear. This study aimed to explore the roles of ZFAS1 in the radioresistance of NPC. Bioinformatics analysis was conducted to identify the significant factors (ENO2 and miR-7-5p) that contributed to the radioresistance of NPC cells. After performing qRT-PCR analysis, we found that the expression of ZFAS1 and ENO2 was upregulated in NPC cells but that the miR-7-5p expression was downregulated in the same samples. Apart from that, we noticed that ZFAS1 inhibition enhanced the sensitivity of NPC cells to radiation therapy by repressing cell proliferation and promoting cell apoptosis. Subsequently, we found that ZFAS1 could sponge miR-7-5p to upregulate ENO2, which was the target of miR-7-5p. Experimental results also indicated that the suppression of miR-7-5p inhibited the sensitivity of NPC cells to radiation therapy, thereby suppressing ENO2 expression. Overall, our findings suggested that ZFAS1 contributed to the radioresistance of NPC cells by regulating the miR-7-5p/ENO2 axis and that ZFAS1 might be a potential therapeutic target for addressing the radioresistance of NPC cells.

摘要

先前的研究表明,lncRNA ZFAS1 可以通过抑制其下游靶轴来促进鼻咽癌(NPC)。然而,ZFAS1 与耐辐射 NPC 细胞之间的关联尚不清楚。本研究旨在探讨 ZFAS1 在 NPC 耐辐射中的作用。进行了生物信息学分析,以确定对 NPC 细胞耐辐射有贡献的显著因素(ENO2 和 miR-7-5p)。进行 qRT-PCR 分析后,我们发现 NPC 细胞中 ZFAS1 和 ENO2 的表达上调,而相同样本中 miR-7-5p 的表达下调。除此之外,我们注意到 ZFAS1 抑制通过抑制细胞增殖和促进细胞凋亡来增强 NPC 细胞对放射治疗的敏感性。随后,我们发现 ZFAS1 可以通过海绵吸附 miR-7-5p 来上调 ENO2,这是 miR-7-5p 的靶标。实验结果还表明,抑制 miR-7-5p 抑制了 NPC 细胞对放射治疗的敏感性,从而抑制了 ENO2 的表达。总体而言,我们的研究结果表明,ZFAS1 通过调节 miR-7-5p/ENO2 轴促进 NPC 细胞的耐辐射性,并且 ZFAS1 可能是解决 NPC 细胞耐辐射性的潜在治疗靶点。