{"title":"Overexpression of <i>LINC00880</i> promotes colorectal cancer growth.","authors":"Ge Gao, Peiwen Xu, Chunyu Yang, Mengyuan Qian, Qingwen Wang, Surui Yao, Yuan Yin, Zhaohui Huang, Zehua Bian","doi":"10.21037/tcr-2025-54","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Research has revealed that long non-coding RNAs (lncRNAs) are intimately associated with the occurrence, development, and metastasis of tumors through their regulation of gene expression. The lncRNA <i>LINC00880</i> is important for colorectal cancer (CRC) occurrence and development. Our research aimed to explore the roles of <i>LINC00880</i> in CRC progression.</p><p><strong>Methods: </strong>The expression of <i>LINC00880</i> in CRC cells and tissues was first measured using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and the prognosis of CRC patients was then investigated using the Kaplan-Meier method. The impacts of <i>LINC00880</i> on CRC growth were evaluated by a series of <i>in vitro</i> and <i>in vivo</i> assays. Mechanistically, RNA sequencing (RNA-seq) technology and transcriptome analysis experiments were employed to validate the impact of <i>LINC00880</i> on cell cycle pathway.</p><p><strong>Results: </strong>In this study, we have demonstrated, for the first time, that <i>LINC00880</i> is significantly overexpressed in CRC and is associated with poor patient survival. Functional assays indicated that <i>LINC00880</i> promotes the growth of CRC cells both <i>in vitro</i> and <i>in vivo</i>. Furthermore, RNA-seq has revealed the impact of <i>LINC00880</i> on the cell cycle and DNA replication pathways, and identified MCM3 as a potential downstream target of <i>LINC00880</i>.</p><p><strong>Conclusions: </strong>Our findings indicate that <i>LINC00880</i> is upregulated in CRC and promotes tumor growth.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 5","pages":"2926-2939"},"PeriodicalIF":1.5000,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12169995/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Translational cancer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.21037/tcr-2025-54","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/5/23 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Research has revealed that long non-coding RNAs (lncRNAs) are intimately associated with the occurrence, development, and metastasis of tumors through their regulation of gene expression. The lncRNA LINC00880 is important for colorectal cancer (CRC) occurrence and development. Our research aimed to explore the roles of LINC00880 in CRC progression.
Methods: The expression of LINC00880 in CRC cells and tissues was first measured using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and the prognosis of CRC patients was then investigated using the Kaplan-Meier method. The impacts of LINC00880 on CRC growth were evaluated by a series of in vitro and in vivo assays. Mechanistically, RNA sequencing (RNA-seq) technology and transcriptome analysis experiments were employed to validate the impact of LINC00880 on cell cycle pathway.
Results: In this study, we have demonstrated, for the first time, that LINC00880 is significantly overexpressed in CRC and is associated with poor patient survival. Functional assays indicated that LINC00880 promotes the growth of CRC cells both in vitro and in vivo. Furthermore, RNA-seq has revealed the impact of LINC00880 on the cell cycle and DNA replication pathways, and identified MCM3 as a potential downstream target of LINC00880.
Conclusions: Our findings indicate that LINC00880 is upregulated in CRC and promotes tumor growth.
期刊介绍:
Translational Cancer Research (Transl Cancer Res TCR; Print ISSN: 2218-676X; Online ISSN 2219-6803; http://tcr.amegroups.com/) is an Open Access, peer-reviewed journal, indexed in Science Citation Index Expanded (SCIE). TCR publishes laboratory studies of novel therapeutic interventions as well as clinical trials which evaluate new treatment paradigms for cancer; results of novel research investigations which bridge the laboratory and clinical settings including risk assessment, cellular and molecular characterization, prevention, detection, diagnosis and treatment of human cancers with the overall goal of improving the clinical care of cancer patients. The focus of TCR is original, peer-reviewed, science-based research that successfully advances clinical medicine toward the goal of improving patients'' quality of life. The editors and an international advisory group of scientists and clinician-scientists as well as other experts will hold TCR articles to the high-quality standards. We accept Original Articles as well as Review Articles, Editorials and Brief Articles.