{"title":"CBX4/miR-190 regulatory loop inhibits lung cancer metastasis.","authors":"Jian Wang, Xiang Zhu, Yue Yu, Jie Ge, Wei Chen, Wengui Xu, Wen Zhou","doi":"10.1111/1759-7714.15415","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Lung cancer is one of the major threats to human life worldwide. MiR-190 has been found to perform essential roles in multiple cancer progression; however, there have been no studies focused on its function and underlying regulatory mechanism in lung cancer.</p><p><strong>Method: </strong>The miR-190 expression was detected by real-time quantitative polymerase chain reaction (RT-qPCR). The cell functional experiments, including cell counting kit-8 (CCK-8), colony formation and transwell assay were conducted in vitro, as well as animal experiments performed in vivo. The regulation and potential binding sites of CBX4 on miR-190 were predicted by TCGA data set and JASPAR website and verified by ChIP assay and dual-luciferase reporter assay. The prospects binding site of miR-190-3p on CBX4 3'UTR region was predicted by StarBase and verified by dual-luciferase reporter assay.</p><p><strong>Results: </strong>MiR-190 was decreased in lung cancer cells. The overexpression of miR-190 had no effects on cell proliferation, but significantly inhibited cancer metastasis both in vitro and in vivo. Moreover, miR-190 expression could be transcriptionally inhibited by CBX4, and CBX4 was the direct target of miR-190-3p.</p><p><strong>Conclusion: </strong>MiR-190 served as a cancer metastasis inhibitor in lung cancer and formed a regulatory loop with CBX4. These findings provided emerging insights into therapeutic targets and strategies for metastatic lung cancer.</p>","PeriodicalId":23338,"journal":{"name":"Thoracic Cancer","volume":" ","pages":"1889-1896"},"PeriodicalIF":2.3000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462972/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Thoracic Cancer","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/1759-7714.15415","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/8/4 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Lung cancer is one of the major threats to human life worldwide. MiR-190 has been found to perform essential roles in multiple cancer progression; however, there have been no studies focused on its function and underlying regulatory mechanism in lung cancer.
Method: The miR-190 expression was detected by real-time quantitative polymerase chain reaction (RT-qPCR). The cell functional experiments, including cell counting kit-8 (CCK-8), colony formation and transwell assay were conducted in vitro, as well as animal experiments performed in vivo. The regulation and potential binding sites of CBX4 on miR-190 were predicted by TCGA data set and JASPAR website and verified by ChIP assay and dual-luciferase reporter assay. The prospects binding site of miR-190-3p on CBX4 3'UTR region was predicted by StarBase and verified by dual-luciferase reporter assay.
Results: MiR-190 was decreased in lung cancer cells. The overexpression of miR-190 had no effects on cell proliferation, but significantly inhibited cancer metastasis both in vitro and in vivo. Moreover, miR-190 expression could be transcriptionally inhibited by CBX4, and CBX4 was the direct target of miR-190-3p.
Conclusion: MiR-190 served as a cancer metastasis inhibitor in lung cancer and formed a regulatory loop with CBX4. These findings provided emerging insights into therapeutic targets and strategies for metastatic lung cancer.
期刊介绍:
Thoracic Cancer aims to facilitate international collaboration and exchange of comprehensive and cutting-edge information on basic, translational, and applied clinical research in lung cancer, esophageal cancer, mediastinal cancer, breast cancer and other thoracic malignancies. Prevention, treatment and research relevant to Asia-Pacific is a focus area, but submissions from all regions are welcomed. The editors encourage contributions relevant to prevention, general thoracic surgery, medical oncology, radiology, radiation medicine, pathology, basic cancer research, as well as epidemiological and translational studies in thoracic cancer. Thoracic Cancer is the official publication of the Chinese Society of Lung Cancer, International Chinese Society of Thoracic Surgery and is endorsed by the Korean Association for the Study of Lung Cancer and the Hong Kong Cancer Therapy Society.
The Journal publishes a range of article types including: Editorials, Invited Reviews, Mini Reviews, Original Articles, Clinical Guidelines, Technological Notes, Imaging in thoracic cancer, Meeting Reports, Case Reports, Letters to the Editor, Commentaries, and Brief Reports.