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SNHG7/miR-9-5p/DPP4 竞争 RNA 网络通过激活 PI3K/Akt 在甲状腺癌细胞生长和碘抵抗中的作用。

Roles of the SNHG7/microRNA‑9‑5p/DPP4 ceRNA network in the growth and I resistance of thyroid carcinoma cells through PI3K/Akt activation.

机构信息

Department of Thyroid Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

出版信息

Oncol Rep. 2021 Apr;45(4). doi: 10.3892/or.2021.7954. Epub 2021 Mar 2.

DOI:10.3892/or.2021.7954
PMID:33649840
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7877006/
Abstract

Radioactive iodine (RAI, I) therapy is the main treatment for thyroid carcinoma (TC). Long noncoding RNA (lncRNA)/microRNA (miR) competing endogenous RNA (ceRNA) networks have aroused great interest for their roles in gene expression. The present study aimed to investigate the effect of lncRNA SNHG7 on the growth and I resistance of TC. Differentially expressed lncRNAs in TC and paracancerous tissues were analyzed. The binding of miR‑9‑5p with small nucleolar RNA host gene 7 (SNHG7) and dipeptidyl‑peptidase 4 (DPP4) was identified. Gain‑ and loss‑of‑function analyses of SNHG7 and miR‑9‑5p were performed to determine their effects on the growth and I resistance of TC cells. The activity of the PI3K/Akt pathway was evaluated. Consequently, upregulated SNHG7 was revealed in TC tissues and correlated with I resistance. Silencing of SNHG7 or overexpressing miR‑9‑5p inhibited the growth and I resistance of TC cells. SNHG7 acted as a ceRNA of miR‑9‑5p to enhance DPP4 expression. Overexpressed SNHG7 increased DPP4 expression and activated the PI3K/Akt signaling pathway by sponging miR‑9‑5p. The results were reproduced . In summary, the present study provided evidence that the SNHG7/miR‑9‑5p/DPP4 ceRNA network could promote the growth and I resistance of TC cells via PI3K/Akt activation. The present study may offer novel options for TC treatment.

摘要

放射性碘(RAI,I)治疗是甲状腺癌(TC)的主要治疗方法。长链非编码 RNA(lncRNA)/microRNA(miR)竞争内源性 RNA(ceRNA)网络因其在基因表达中的作用而引起了极大的兴趣。本研究旨在探讨 lncRNA SNHG7 对 TC 生长和碘抵抗的影响。分析 TC 和癌旁组织中差异表达的 lncRNA。鉴定了 miR-9-5p 与小核仁 RNA 宿主基因 7(SNHG7)和二肽基肽酶 4(DPP4)的结合。进行了 SNHG7 和 miR-9-5p 的增益和缺失功能分析,以确定它们对 TC 细胞生长和碘抵抗的影响。评估了 PI3K/Akt 通路的活性。结果表明,TC 组织中 SNHG7 上调,与碘抵抗相关。沉默 SNHG7 或过表达 miR-9-5p 抑制 TC 细胞的生长和碘抵抗。SNHG7 作为 miR-9-5p 的 ceRNA 增强 DPP4 的表达。过表达的 SNHG7 通过海绵吸附 miR-9-5p 增加 DPP4 的表达并激活 PI3K/Akt 信号通路。结果得以重现。总之,本研究提供了证据表明,SNHG7/miR-9-5p/DPP4 ceRNA 网络可通过激活 PI3K/Akt 促进 TC 细胞的生长和碘抵抗。本研究可能为 TC 的治疗提供新的选择。

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