ArticleOncogenesis2017
MeCP2, a target of miR-638, facilitates gastric cancer cell proliferation through activation of the MEK1/2-ERK1/2 signaling pathway by upregulating GIT1.
Article in Oncogenesis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The trial behind it
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Who cites it
36 citing papers in PubMed, 71 citations in OpenAlex.
- MeCP2 functions as a DNA methylation reader in immune homeostasis and cancer.Frontiers in epigenetics and epigenomics · 2026Review
- Review
- The Epigenetic Reader Methyl-CpG-Binding Protein 2 (MeCP2) Is an Emerging Oncogene in Cancer Biology.Cancers · 2023Review
- Construction of a synthetic methodology-based library and its application in identifying a GIT/PIX protein-protein interaction inhibitor.Nature communications · 2022Article
- Bioinformatics analysis of prognostic value and immunological role of MeCP2 in pan-cancer.Scientific reports · 2022Article
- Article
- Heat Shock Procedure Affects Cell Division-Associated Genes in Gynogenetic Manipulation.Marine biotechnology (New York, N.Y.) · 2022Article
- Article
- MeCP2 confers 5-fluorouracil resistance in gastric cancer via upregulating the NOX4/PKM2 pathway.Cancer cell international · 2022Article
- G-Protein-Coupled Receptor Kinase-Interacting Protein 1 (GIT1) Promotes Head and Neck Squamous Cell Carcinoma Metastases via Activating the PI3K/AKT/mTOR Signal Pathway.Computational and mathematical methods in medicine · 2022Article
- MECP2 promotes the migration and invasion of gastric cancer cells by modulating the Notch1/c-Myc/mTOR signaling pathways by suppressing FBXW7 transcription.American journal of cancer research · 2022Article
- GIT1 overexpression promotes epithelial-mesenchymal transition and predicts poor prognosis in hepatocellular carcinoma.Bioengineered · 2021Article
- miR-363-3p induces EMT via the Wnt/β-catenin pathway in glioma cells by targeting CELF2.Journal of cellular and molecular medicine · 2021Article
- Methyl CpG binding protein 2 promotes colorectal cancer metastasis by regulating NCancer science · 2021Article
- MicroRNA-665 facilitates cell proliferation and represses apoptosis through modulating Wnt5a/β-Catenin and Caspase-3 signaling pathways by targeting TRIM8 in LUSC.Cancer cell international · 2021Article
- Regulation of DNA methylation machinery by epi-miRNAs in human cancer: emerging new targets in cancer therapy.Cancer gene therapy · 2021Review
- Overview of host miRNA properties and their association with epigenetics, long non-coding RNAs, and Xeno-infectious factors.Cell & bioscience · 2021Review
- Circular RNA Protein Tyrosine Kinase 2 Promotes Cell Proliferation, Migration and Suppresses ApoptosisFrontiers in oncology · 2021Article
- LINC00518 Promotes Cell Proliferation by Regulating the Cell Cycle of Lung Adenocarcinoma Through miR-185-3p Targeting MECP2.Frontiers in oncology · 2021Article
- POLR2A Promotes the Proliferation of Gastric Cancer Cells by Advancing the Overall Cell Cycle Progression.Frontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methyl-CpG binding protein 2 (MeCP2) is involved in the carcinogenesis and progression of multiple types of cancer. However, its precise role in gastric cancer (GC) and the relevant molecular mechanism remain unknown. In the present study, we found that miR-638 levels were lower in GC tissues and GC cell lines than in adjacent normal tissues and normal gastric epithelial cell lines, respectively. Low miR-638 levels were associated with poor tumor differentiation, tumor size and lymph node metastasis. MeCP2 expression levels were higher in GC tissues than in adjacent normal tissues. It was found that miR-638 inhibited GC cell proliferation, colony formation, G1-S transition and tumor growth, and induced cell apoptosis by directly targeting MeCP2. MeCP2 promoted GC cell proliferation, colony formation and G1-S cell-cycle transition, and suppressed apoptosis. Molecular mechanistic investigations were performed using an integrated approach with a combination of microarray analysis, chromatin immunoprecipitation sequencing and a reporter gene assay. The results showed that MeCP2 bound to the methylated CpG islands of G-protein-coupled receptor kinase-interacting protein 1 (GIT1) promoter and upregulated its expression, thereby activating the MEK1/2-ERK1/2 signaling pathway and promoting GC cell proliferation. Taken together, our study demonstrates that MeCP2, a target of miR-638, facilitates GC cell proliferation and induces cell-cycle progression through activation of the MEK1/2-ERK1/2 signaling pathway by upregulating GIT1. The findings suggest that MeCP2 plays a significant role in GC progression, and may serve as a potential target for GC therapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.