Downregulation of Long Noncoding RNA Myocardial Infarction Associated Transcript Suppresses Cell Proliferation, Migration, Invasion, and Glycolysis by Regulation of miR-488-3p/IGF1R Pathway in Colorectal Cancer.
Background: Colorectal cancer (CRC) is a significant public problem and the third cause of cancer-induced death all over the world. Long noncoding RNA (lncRNA) has been reported as a vital mediator in human cancer. However, the precise role of lncRNA myocardial infarction associated transcript (MIAT...
| Publicado en: | Cancer Biotherapy & Radiopharmaceuticals Vol. 37; no. 10; pp. 927 - 939 |
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| Autores principales: | , , , , , |
| Formato: | research tables/charts Journal Article |
| Publicado: |
Mary Ann Liebert, Inc.
Dec2022
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| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=160777643&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 160777643 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 10849785 N3A jtl: Cancer Biotherapy & Radiopharmaceuticals issn: 10849785 maglogo: N pubinfo: dt: Dec2022 vid: 37 iid: 10 pid: 1365 pub: Mary Ann Liebert, Inc. place: New Rochelle, New York artinfo: ui: 160777643 160777643 160777643 10.1089/cbr.2020.3671 160777643 ppf: 927 ppct: 12 formats: tig: atl: Downregulation of Long Noncoding RNA Myocardial Infarction Associated Transcript Suppresses Cell Proliferation, Migration, Invasion, and Glycolysis by Regulation of miR-488-3p/IGF1R Pathway in Colorectal Cancer. aug: au: Liu, Yunhua Peng, Huaiying Shen, Yongxiang Da, Rongfeng Tian, Aihua Guo, Xiaomei affil: Department of Gastroenterology, the First People's Hospital of Tianmen, Hubei, China. sug: subj: Colorectal Neoplasms Cell Migration Assays Cell Proliferation RNA Metabolism Myocardial Infarction Human Descriptive Statistics Data Analysis Software Male Female T-Tests Analysis of Variance Adult Middle Age Aged Aged, 80 and Over Adult: 19-44 years Middle Aged: 45-64 years Aged: 65+ years Aged, 80 & over Male Female ab: Background: Colorectal cancer (CRC) is a significant public problem and the third cause of cancer-induced death all over the world. Long noncoding RNA (lncRNA) has been reported as a vital mediator in human cancer. However, the precise role of lncRNA myocardial infarction associated transcript (MIAT) in CRC is unclear. Materials and Methods: The abundance of MIAT, miR-488-3p, and the type 1 insulin-like growth factor receptor (IGF1R) was measured by real-time quantitative polymerase chain reaction assay. Western blot assay was carried out to assess the protein level in CRC samples or control group. The cell activity, abilities of migration and invasion, and glycolysis were evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT), transwell, and testing glucose consumption and lactate product, correspondingly. The target association between miR-488-3p, MIAT, or IGF1R was predicted and established by bioinformatics tools, dual-luciferase reporter, and RNA pull-down assays, correspondingly. The effects of MIAT silencing in vivo were analyzed by animal experiments. Results: LncRNA MIAT was upregulated in CRC sample and that was positively correlated with IGF1R expression. Loss-of-functional assay suggested that knockdown of MIAT impeded cell activity, migration, invasion, and glycolysis of CRC cells in vivo, along with xenograft growth in vivo. Moreover, silencing of IGF1R inhibited the progression of CRC. Therefore, overexpression of IGF1R could abolish silencing of MIAT-induced effects on CRC cells. Mechanistically, MIAT was a sponge for miR-488-3p, thereby regulating IGF1R expression in CRC. Conclusion: The present study confirmed that the "MIAT/miR-488-3p/IGF1R" pathway was involved in the development of CRC, which may be the target for developing therapeutic approaches for CRC. pubtype: Academic Journal doctype: research tables/charts Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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