ArticleCancer cell international2018
Long non-coding RNA MIAT promotes growth and metastasis of colorectal cancer cells through regulation of miR-132/Derlin-1 pathway.
Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Clinicopathological and Prognostic Significance of Long Non-coding RNA MIAT in Human Cancers: A Review and Meta-Analysis.Frontiers in genetics · 2021Pooled it
- Long non-coding RNAs in the crosstalk between diabetes and colorectal cancer: molecular mechanisms and endocrine pathways.Frontiers in molecular biosciences · 2026Review
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- LDA-SCGB: inferring lncRNA-disease associations based on condensed gradient boosting.BMC bioinformatics · 2025Article
- MIAT: A pivotal oncogenic long noncoding RNA tunning the hallmarks of solid malignancies.Translational oncology · 2025Article
- Clinical Analysis of Pyroptosis-Related Long Non-Coding RNAs MIAT and Gm15441 in Colorectal Cancer Patients with a History of Ulcerative Colitis.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Article
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- Novel role of lncRNAs regulatory network in papillary thyroid cancer.Biochemistry and biophysics reports · 2024Review
- Restricting Colorectal Cancer Cell Metabolism with Metformin: An Integrated Transcriptomics Study.Cancers · 2024Article
- Competitive endogenous RNA networks: Decoding the role of long non-coding RNAs and circular RNAs in colorectal cancer chemoresistance.Journal of cellular and molecular medicine · 2024Review
- LncRNA-MIAT activates hepatic stellate cells via regulating Hippo pathway and epithelial-to-mesenchymal transition.Communications biology · 2023Article
- Mesenchymal Stem Cell Derived Exosomes Suppress Neuronal Cell Ferroptosis Via lncGm36569/miR-5627-5p/FSP1 Axis in Acute Spinal Cord Injury.Stem cell reviews and reports · 2022Article
- MicroRNA-375-3p Suppresses Upper Tract Urothelial Carcinoma Cell Migration and Invasion via Targeting Derlin-1.Cancers · 2022Article
- Comprehensive Analyses of Stromal-Immune Score-Related Competing Endogenous RNA Networks In Colon Adenocarcinoma.Disease markers · 2022Article
- LncAABR07025387.1 Enhances Myocardial Ischemia/Reperfusion InjuryFrontiers in cell and developmental biology · 2022Article
- LncRNA MIAT Inhibits MPPNeurochemical research · 2021Article
- Effects of long non-coding RNA myocardial infarction-associated transcript on retinal neovascularization in a newborn mouse model of oxygen-induced retinopathy.Neural regeneration research · 2021Article
- Molecular mechanisms of the microRNA-132 during tumor progressions.Cancer cell international · 2021Review
- Roles of long non‑coding RNA in osteoarthritis (Review).International journal of molecular medicine · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveRecently, long non-coding RNA (lncRNA) MIAT has been demonstrated as an oncogenic gene in several types of cancer. However, the role and mechanism of MIAT in colorectal cancer (CRC) have not been investigated.
methodsReal-time PCR was used to measure MIAT expression in CRC tissues and cells. Small interfering RNA specific for MIAT (si-MIAT) was used to down-regulate MIAT expression in CRC cells. The interaction of MIAT and miR-132 was measured by RNA pull-down assay. The effect of si-MIAT on CRC cells apoptosis and metastasis were measured by flow cytometry assay, invasion and migration assay, respectively.
resultsIn present study, we found that MIAT was highly expressed in CRC tissues and cells. MIAT knockdown inhibited proliferation, migration and invasion and enhanced apoptosis of CRC cells. Further, we demonstrated that MIAT acted as a competing endogenous RNA for miR-132, antagonized its functions, and resulted in the de-repression of its target gene Derlin-1, which acted as an oncogene in promoting growth and metastasis of CRC cells. In LOVO and SW480 cells with si-MIAT, miR-132 inhibitor resulted in an increase of cell proliferation, migration and invasion and a decrease of cell apoptosis, which was partially abolished by transfection of Derlin-1 shRNA.
conclusionsOur data indicated that highly expressed MIAT was an oncogenic lncRNA that promoted the growth and metastasis of CRC through miR-132/Derlin-1 axis.
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