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
| Autor: | Yongxiang Shen, Rongfeng Da, Huaiying Peng, Xiaomei Guo, Yunhua Liu, Aihua Tian |
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| Rok vydání: | 2022 |
| Předmět: |
0301 basic medicine
Pharmacology Cancer Research Gene knockdown Cell growth General Medicine Biology 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Real-time polymerase chain reaction Oncology Growth factor receptor Downregulation and upregulation 030220 oncology & carcinogenesis microRNA Cancer research Gene silencing Radiology Nuclear Medicine and imaging Insulin-like growth factor 1 receptor |
| Zdroj: | Cancer Biotherapy and Radiopharmaceuticals. 37:927-938 |
| ISSN: | 1557-8852 1084-9785 |
| DOI: | 10.1089/cbr.2020.3671 |
| Popis: | Background: Colorectal cancer (CRC) is a significant public problem and the third cause of cancer-induced death all over the world. In addition, 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. 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. The 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. |
| Databáze: | OpenAIRE |
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