Zhigang Luo, Zhiyi Han, F. Shou, Yangchao Li, Yang Chen
{"title":"LINC00958 accelerates cell proliferation and migration in non-small cell lung cancer through JNK/c-JUN signaling.","authors":"Zhigang Luo, Zhiyi Han, F. Shou, Yangchao Li, Yang Chen","doi":"10.1089/hum.2019.115","DOIUrl":null,"url":null,"abstract":"Non-small cell lung cancer (NSCLC) denotes the commonest type of lung cancers with high mortality globally. Long non-coding RNAs (lncRNAs) with differential expression have been indicated to be participants in the pathogenesis and development of cancer. However, the precise role of lncRNAs in NSCLC is still largely obscure. In this study, we explored a newly-discovered intergenic lncRNA LINC00958 in NSCLC. First of all, the online databases suggested that LINC00958 was low expressed in human normal lung tissues but upregulated in LUSC tissues. Besides, the upregulation of LINC00958 in both LUAD and LUSC cell lines was easily found when comparing to the normal BEAS-2B cells. In addition, we elucidated that knockdown of LINC00958 led to impaired proliferation, induced apoptosis and hampered migration in LUAD cells. Moreover, a typical oncogenic pathway, JNK signaling, was verified to be involved in LINC00958-contributed LUAD development. Of note, we explained that LINC00958 exerted the tumor-promoting function in LUAD by enhancing the transactivation of p-c-JUN through activating JNK signaling. Meanwhile, we also revealed that LINC00958 was transcriptionally regulated by c-JUN. Additionally, above findings were also suitable for LUSC cells. By and large, our work illustrated that LINC00958 facilitates tumorigenesis in NSCLC by activating JNK/c-JUN signaling pathway, indicating a new road for diagnosis and treatment of both LUAD and LUSC.","PeriodicalId":13126,"journal":{"name":"Human Gene Therapy Methods","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/hum.2019.115","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Human Gene Therapy Methods","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1089/hum.2019.115","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Immunology and Microbiology","Score":null,"Total":0}
引用次数: 5
Abstract
Non-small cell lung cancer (NSCLC) denotes the commonest type of lung cancers with high mortality globally. Long non-coding RNAs (lncRNAs) with differential expression have been indicated to be participants in the pathogenesis and development of cancer. However, the precise role of lncRNAs in NSCLC is still largely obscure. In this study, we explored a newly-discovered intergenic lncRNA LINC00958 in NSCLC. First of all, the online databases suggested that LINC00958 was low expressed in human normal lung tissues but upregulated in LUSC tissues. Besides, the upregulation of LINC00958 in both LUAD and LUSC cell lines was easily found when comparing to the normal BEAS-2B cells. In addition, we elucidated that knockdown of LINC00958 led to impaired proliferation, induced apoptosis and hampered migration in LUAD cells. Moreover, a typical oncogenic pathway, JNK signaling, was verified to be involved in LINC00958-contributed LUAD development. Of note, we explained that LINC00958 exerted the tumor-promoting function in LUAD by enhancing the transactivation of p-c-JUN through activating JNK signaling. Meanwhile, we also revealed that LINC00958 was transcriptionally regulated by c-JUN. Additionally, above findings were also suitable for LUSC cells. By and large, our work illustrated that LINC00958 facilitates tumorigenesis in NSCLC by activating JNK/c-JUN signaling pathway, indicating a new road for diagnosis and treatment of both LUAD and LUSC.
期刊介绍:
Human Gene Therapy is the premier, multidisciplinary journal covering all aspects of gene therapy. The Journal publishes in-depth coverage of DNA, RNA, and cell therapies by delivering the latest breakthroughs in research and technologies. Human Gene Therapy provides a central forum for scientific and clinical information, including ethical, legal, regulatory, social, and commercial issues, which enables the advancement and progress of therapeutic procedures leading to improved patient outcomes, and ultimately, to curing diseases.
The Journal is divided into three parts. Human Gene Therapy, the flagship, is published 12 times per year. HGT Methods, a bimonthly journal, focuses on the applications of gene therapy to product testing and development. HGT Clinical Development, a quarterly journal, serves as a venue for publishing data relevant to the regulatory review and commercial development of cell and gene therapy products.