LMCD1-AS1通过海绵miR-873-3p促进宫颈癌细胞增殖和EMT。

IF 1.5 4区 医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
Miao Liang, Yongkang Li, Cheng Chen
{"title":"LMCD1-AS1通过海绵miR-873-3p促进宫颈癌细胞增殖和EMT。","authors":"Miao Liang,&nbsp;Yongkang Li,&nbsp;Cheng Chen","doi":"10.1615/CritRevEukaryotGeneExpr.2022042882","DOIUrl":null,"url":null,"abstract":"<p><p>Long non-coding RNA LMCD1 antisense RNA 1 (LMCD1-AS1) has recently been reported to participate in the pathogenesis of several tumors, including thyroid cancer and osteosarcoma. However, the clinical significance of LMCD1-AS1 and the related biological function have not been reported in cervical cancer (CC). In this study, we observed that LMCD1-AS1 expression was highly expressed in CC specimens compared with adjacent normal specimens using quantitative real-time PCR. Chi-square test showed that high LMCD1-AS1 expression was correlated with FIGO stage and lymph node metastasis. Kaplan-Meier survival analysis showed poor prognosis with high LMCD1-AS1 expression. Moreover, FIGO stage, lymph node metastasis and high LMCD1-AS1 expression could be independent prognostic factors for the patients with CC. Functionally, knockdown of LMCD1-AS1 suppressed the proliferation, migration and invasion of two CC cell lines (HeLa and CaSki) cells by CCK-8 assay, colony formation assay, and Transwell assay. Knockdown of LMCD1-AS1 upregulated E-cadherin expression and downregulated the expression of PCNA, N-cadherin, and imentin in HeLa and CaSki cells. Luciferase reporter assay and RIP assay were conducted to evaluate the downstream molecular mechanisms of LMCD1-AS1. LMCD1-AS1 possesses a putative miR-873-3p-binding site and confirmed the negative correlation between them in CC tissues. Moreover, overexpression of LMCD1-AS1 promoted CC cell proliferation and EMT process through the regulation of miR-873-3p. In addition, depletion of LMCD1-AS1 reduced tumor growth and Ki-67 protein expression. In summary, our findings indicate that LMCD1-AS1 might exert an oncogenic role in CC and targeting LMCD1-AS1 might be a promising therapeutic target for CC treatment.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"33 2","pages":"13-25"},"PeriodicalIF":1.5000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"LMCD1-AS1 Facilitates Cell Proliferation and EMT by Sponging miR-873-3p in Cervical Cancer.\",\"authors\":\"Miao Liang,&nbsp;Yongkang Li,&nbsp;Cheng Chen\",\"doi\":\"10.1615/CritRevEukaryotGeneExpr.2022042882\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Long non-coding RNA LMCD1 antisense RNA 1 (LMCD1-AS1) has recently been reported to participate in the pathogenesis of several tumors, including thyroid cancer and osteosarcoma. However, the clinical significance of LMCD1-AS1 and the related biological function have not been reported in cervical cancer (CC). In this study, we observed that LMCD1-AS1 expression was highly expressed in CC specimens compared with adjacent normal specimens using quantitative real-time PCR. Chi-square test showed that high LMCD1-AS1 expression was correlated with FIGO stage and lymph node metastasis. Kaplan-Meier survival analysis showed poor prognosis with high LMCD1-AS1 expression. Moreover, FIGO stage, lymph node metastasis and high LMCD1-AS1 expression could be independent prognostic factors for the patients with CC. Functionally, knockdown of LMCD1-AS1 suppressed the proliferation, migration and invasion of two CC cell lines (HeLa and CaSki) cells by CCK-8 assay, colony formation assay, and Transwell assay. Knockdown of LMCD1-AS1 upregulated E-cadherin expression and downregulated the expression of PCNA, N-cadherin, and imentin in HeLa and CaSki cells. Luciferase reporter assay and RIP assay were conducted to evaluate the downstream molecular mechanisms of LMCD1-AS1. LMCD1-AS1 possesses a putative miR-873-3p-binding site and confirmed the negative correlation between them in CC tissues. Moreover, overexpression of LMCD1-AS1 promoted CC cell proliferation and EMT process through the regulation of miR-873-3p. In addition, depletion of LMCD1-AS1 reduced tumor growth and Ki-67 protein expression. In summary, our findings indicate that LMCD1-AS1 might exert an oncogenic role in CC and targeting LMCD1-AS1 might be a promising therapeutic target for CC treatment.</p>\",\"PeriodicalId\":56317,\"journal\":{\"name\":\"Critical Reviews in Eukaryotic Gene Expression\",\"volume\":\"33 2\",\"pages\":\"13-25\"},\"PeriodicalIF\":1.5000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Critical Reviews in Eukaryotic Gene Expression\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2022042882\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOTECHNOLOGY & APPLIED MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Critical Reviews in Eukaryotic Gene Expression","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2022042882","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
引用次数: 2

摘要

长链非编码RNA LMCD1反义RNA 1 (LMCD1- as1)最近被报道参与多种肿瘤的发病机制,包括甲状腺癌和骨肉瘤。然而,LMCD1-AS1在宫颈癌(CC)中的临床意义及相关生物学功能尚未见报道。在本研究中,我们通过实时荧光定量PCR观察到,与邻近的正常标本相比,LMCD1-AS1在CC标本中高表达。卡方检验显示LMCD1-AS1高表达与FIGO分期及淋巴结转移相关。Kaplan-Meier生存分析显示,LMCD1-AS1高表达患者预后较差。此外,FIGO分期、淋巴结转移和LMCD1-AS1高表达可能是CC患者预后的独立因素。CCK-8实验、集落形成实验和Transwell实验显示,LMCD1-AS1敲低在功能上抑制了两种CC细胞系(HeLa和CaSki)细胞的增殖、迁移和侵袭。敲低LMCD1-AS1可上调HeLa和CaSki细胞中E-cadherin的表达,下调PCNA、N-cadherin和imentin的表达。采用荧光素酶报告基因法和RIP法研究LMCD1-AS1的下游分子机制。LMCD1-AS1具有推测的mir -873-3p结合位点,并证实它们在CC组织中呈负相关。此外,LMCD1-AS1过表达通过调控miR-873-3p促进CC细胞增殖和EMT过程。此外,LMCD1-AS1的缺失降低了肿瘤生长和Ki-67蛋白的表达。综上所述,我们的研究结果表明LMCD1-AS1可能在CC中发挥致癌作用,靶向LMCD1-AS1可能是CC治疗的一个有希望的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
LMCD1-AS1 Facilitates Cell Proliferation and EMT by Sponging miR-873-3p in Cervical Cancer.

Long non-coding RNA LMCD1 antisense RNA 1 (LMCD1-AS1) has recently been reported to participate in the pathogenesis of several tumors, including thyroid cancer and osteosarcoma. However, the clinical significance of LMCD1-AS1 and the related biological function have not been reported in cervical cancer (CC). In this study, we observed that LMCD1-AS1 expression was highly expressed in CC specimens compared with adjacent normal specimens using quantitative real-time PCR. Chi-square test showed that high LMCD1-AS1 expression was correlated with FIGO stage and lymph node metastasis. Kaplan-Meier survival analysis showed poor prognosis with high LMCD1-AS1 expression. Moreover, FIGO stage, lymph node metastasis and high LMCD1-AS1 expression could be independent prognostic factors for the patients with CC. Functionally, knockdown of LMCD1-AS1 suppressed the proliferation, migration and invasion of two CC cell lines (HeLa and CaSki) cells by CCK-8 assay, colony formation assay, and Transwell assay. Knockdown of LMCD1-AS1 upregulated E-cadherin expression and downregulated the expression of PCNA, N-cadherin, and imentin in HeLa and CaSki cells. Luciferase reporter assay and RIP assay were conducted to evaluate the downstream molecular mechanisms of LMCD1-AS1. LMCD1-AS1 possesses a putative miR-873-3p-binding site and confirmed the negative correlation between them in CC tissues. Moreover, overexpression of LMCD1-AS1 promoted CC cell proliferation and EMT process through the regulation of miR-873-3p. In addition, depletion of LMCD1-AS1 reduced tumor growth and Ki-67 protein expression. In summary, our findings indicate that LMCD1-AS1 might exert an oncogenic role in CC and targeting LMCD1-AS1 might be a promising therapeutic target for CC treatment.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Critical Reviews in Eukaryotic Gene Expression
Critical Reviews in Eukaryotic Gene Expression 生物-生物工程与应用微生物
CiteScore
2.70
自引率
0.00%
发文量
67
审稿时长
1 months
期刊介绍: Critical ReviewsTM in Eukaryotic Gene Expression presents timely concepts and experimental approaches that are contributing to rapid advances in our mechanistic understanding of gene regulation, organization, and structure within the contexts of biological control and the diagnosis/treatment of disease. The journal provides in-depth critical reviews, on well-defined topics of immediate interest, written by recognized specialists in the field. Extensive literature citations provide a comprehensive information resource. Reviews are developed from an historical perspective and suggest directions that can be anticipated. Strengths as well as limitations of methodologies and experimental strategies are considered.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信