LncRNA EGOT/miR-211-5p Affected Radiosensitivity of Rectal Cancer by Competitively Regulating ErbB4.
LncRNA EGOT/miR-211-5p Affected Radiosensitivity of Rectal Cancer by Competitively Regulating ErbB4.
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DOI：
10.2147/ott.s256989
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发表时间：
2021
影响因子：
4
通讯作者：
Jiang Z
中科院分区：
文献类型：
--
作者：
Li C;Liu H;Wei R;Liu Z;Chen H;Guan X;Zhao Z;Wang X;Jiang Z
长的非编码核糖核酸(LncRNAs)参与癌症的发展，并影响对放射治疗的反应。本研究旨在探讨lncRNA EGOT在直肠癌放射增敏中的作用机制。采用定量逆转录聚合酶链式反应检测直肠癌组织和细胞中EGOT、miR-211-5p和ErbB4基因的表达。Western印迹法检测ErbB4蛋白表达。用双荧光素酶报告实验和核糖核酸免疫沉淀(RIP)方法证实了EGOT与miR-211-5p或miR-211-5p与ErbB4的相互作用。利用转基因技术分别下调和上调EGOT和miR-211-5p在直肠癌细胞中的表达。采用四甲基偶氮唑盐比色法、集落形成法和流式细胞术检测EGOT和miR-211-5P对直肠癌细胞增殖、侵袭、迁移和凋亡的影响。EGOT在直肠癌组织和细胞中表达上调，且与病理分期有关。EGOT基因敲除抑制直肠癌细胞的增殖和集落形成，并诱导直肠癌细胞的凋亡。此外，EGOT基因敲除显著增强了体内外放疗对直肠癌的疗效。此外，EGOT被发现作为miR-211-5P的海绵，ErbB4是miR-211-5P的下游靶标。EGOT通过调节miR-211-5p增强ErbB4的表达。MIR-211-5P抑制剂恢复了EGOT基因敲除对直肠癌放射敏感性的影响。EGOT下调可通过调节miR-211-5p/ErbB4轴抑制直肠癌细胞的生长，提高直肠癌细胞的放射敏感性。EGOT可能成为直肠癌治疗的新靶点。
Long non-coding ribonucleic acids (lncRNAs) are involved in the progression of cancers and affect the response to radiation therapy. This study was to investigate the mechanism of lncRNA EGOT in the radiosensitivity of rectal cancer. The mRNA expression of EGOT, miR-211-5p and ErbB4 in rectal cancer tissues and cells was detected by qRT-PCR. The protein expression of ErbB4 was detected by Western blot. Dual-luciferase reporter assay and ribonucleic acid immunoprecipitation (RIP) were used to confirm the interaction between EGOT and miR-211-5p or miR-211-5p and ErbB4. Transfection technology was used to down-regulate and up-regulate the expression of EGOT and miR-211-5p in rectal cancer cells, respectively. MTT, colony formation and flow cytometry were used to detect the effect of EGOT and miR-211-5p on proliferation, invasion, migration and apoptosis of rectal cancer cells. The expression of EGOT was up-regulated in rectal cancer tissues and cells, and the expression of EGOT was related to the late stage of pathology. EGOT knockdown inhibited the proliferation and colony formation of rectal cancer cells and induced the apoptosis of rectal cancer cells. Moreover, EGOT knockdown was significantly enhanced the effects of radiotherapy on rectal cancer in vivo and in vitro. Furthermore, EGOT was found to serve as a sponge of miR-211-5p, and ErbB4 was a downstream target of miR-211-5p. EGOT enhanced the expression of ErbB4 by regulating miR-211-5p. MiR-211-5p inhibitor restored the effect of EGOT knockdown on the radiosensitivity of rectal cancer. Down-regulation of EGOT could inhibit the growth of rectal cancer cells by regulating the miR-211-5p/ErbB4 axis and improve the radiosensitivity of rectal cancer cells. EGOT may be a new therapeutic target for rectal cancer.