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长链非编码RNA OIP5-AS1通过miR-27b-3p/TRIM14轴促进口腔鳞状细胞癌对顺铂的耐药性。

Long non-coding RNA OIP5-AS1 contributes to cisplatin resistance of oral squamous cell carcinoma through the miR-27b-3p/TRIM14 axis.

作者信息

Xiao Zhen, Li Jiayi, Jin Qingsong, Liu Dongxiu

机构信息

Oral and Maxillofacial Second Ward, The First Hospital of Qiqihar, Qiqihar, Heilongjiang 161000, P.R. China.

Department of Stomatology, Affiliated Qiqihar Hospital, Southern Medical University, Qiqihar, Heilongjiang 161000, P.R. China.

出版信息

Exp Ther Med. 2021 Apr;21(4):408. doi: 10.3892/etm.2021.9839. Epub 2021 Feb 25.

DOI:10.3892/etm.2021.9839
PMID:33692839
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7938452/
Abstract

Oral squamous cell carcinoma (OSCC) accounts for 90% of oral cavity cancer types, but the overall prognosis for patients with OSCC remains unfavorable. Cisplatin (DDP) is an effective drug in OSCC treatment, but DDP resistance weakens its therapeutic effect. Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) can trigger DDP resistance. The purpose of the current study was to explore the role and mechanism ofOIP5-AS1 in OSCC DDP resistance. In the present study, the expression levels of OIP5-AS1, microRNA (miR)-27b-3p and tripartite motif-containing 14 (TRIM14) were detected by reverse transcription-quantitative PCR. DDP resistance was measured using an MTT assay. Moreover, cell proliferation, migration and invasion were assessed by MTT, Transwell, and Matrigel assays. Protein expression levels of TRIM14, E-cadherin, N-cadherin and Vimentin were detected by western blot analysis. Putative binding sites between miR-27b-3p andOIP5-AS1 or TRIM14werepredicted with starBase and verified using a dual-luciferase reporter assay. The role of OIP5-AS1 in DDP resistance of OSCC was measured using a xenograft tumor model. It was observed that OIP5-AS1 was upregulated in DDP-resistant OSCC cells, and the knockdown of OIP5-AS1 improved DDP sensitivity in DDP-resistant OSCC cells. The present study identified that miR-27b-3p was a target of OIP5-AS1. Furthermore, miR-27b-3p silencing reversed the effect of OIP5-AS1 knockdown on DDP sensitivity in DDP-resistant OSCC cells. TRIM14was shown to be a direct target of miR-27b-3p, and TRIM14 overexpression abolished the effect of miR-27b-3p on DDP sensitivity in DDP-resistant OSCC cells. The results suggested that OIP5-AS1 increased TRIM14 expression by sponging miR-27b-3p. In addition, OIP5-AS1 knockdown enhanced DDP sensitivity of OSCC . Data from the present study indicated that OIP5-AS1 may improve DDP resistance through theupregulationTRIM14 mediated bymiR-27b-3p, providing a possible therapeutic strategy for OSCC treatment.

摘要

口腔鳞状细胞癌（OSCC）占口腔癌类型的90%，但OSCC患者的总体预后仍然不容乐观。顺铂（DDP）是OSCC治疗中的一种有效药物，但DDP耐药性削弱了其治疗效果。Opa相互作用蛋白5反义RNA 1（OIP5-AS1）可引发DDP耐药。本研究的目的是探讨OIP5-AS1在OSCC DDP耐药中的作用及机制。在本研究中，通过逆转录定量PCR检测OIP5-AS1、微小RNA（miR）-27b-3p和含三联基序蛋白14（TRIM14）的表达水平。使用MTT法测定DDP耐药性。此外，通过MTT、Transwell和基质胶实验评估细胞增殖、迁移和侵袭能力。通过蛋白质印迹分析检测TRIM14、E-钙黏蛋白、N-钙黏蛋白和波形蛋白的蛋白表达水平。使用starBase预测miR-27b-3p与OIP5-AS1或TRIM14之间的潜在结合位点，并通过双荧光素酶报告基因实验进行验证。使用异种移植肿瘤模型检测OIP5-AS1在OSCC DDP耐药中的作用。观察到OIP5-AS1在DDP耐药的OSCC细胞中上调，敲低OIP5-AS1可提高DDP耐药的OSCC细胞对DDP的敏感性。本研究确定miR-27b-3p是OIP5-AS1的一个靶点。此外，沉默miR-27b-3p可逆转敲低OIP5-AS1对DDP耐药的OSCC细胞中DDP敏感性的影响。TRIM14被证明是miR-

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739c/7938452/ffbf0b70bf82/etm-21-04-09839-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739c/7938452/dc7fbde40226/etm-21-04-09839-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739c/7938452/885d48b7521c/etm-21-04-09839-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739c/7938452/fadd2af87b4e/etm-21-04-09839-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739c/7938452/b3c13e9c143a/etm-21-04-09839-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739c/7938452/8d924a9841ee/etm-21-04-09839-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/739c/7938452/dbffdfe17877/etm-21-04-09839-g05.jpg
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