ArticleAmerican journal of translational research2018
MiR-106a* inhibits oral squamous cell carcinoma progression by directly targeting MeCP2 and suppressing the Wnt/β-Catenin signaling pathway.
Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- MicroRNA mediated signaling and metabolic reprogramming in oral squamous cell carcinoma.Medical oncology (Northwood, London, England) · 2026Review
- MeCP2 functions as a DNA methylation reader in immune homeostasis and cancer.Frontiers in epigenetics and epigenomics · 2026Review
- C/EBP-β/MeCP2/Wnt Axis Participates in the Testicular Injury in Rats Under Simulated Microgravity Conditions.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- MiR-488-3p facilitates wound healing through CYP1B1-mediated Wnt/β-catenin signaling pathway by targeting MeCP2.Journal of diabetes investigation · 2024Article
- Molecular signaling in cancer stem cells of tongue squamous cell carcinoma: Therapeutic implications and challenges.World journal of stem cells · 2023Review
- The Epigenetic Reader Methyl-CpG-Binding Protein 2 (MeCP2) Is an Emerging Oncogene in Cancer Biology.Cancers · 2023Review
- MiR-422a promotes adipogenesis via MeCP2 downregulation in human bone marrow mesenchymal stem cells.Cellular and molecular life sciences : CMLS · 2023Article
- Research progress and clinical application prospects of miRNAs in oral cancer.Molecular biology reports · 2022Review
- Involvement of RUVBL1 in WNT/Disease markers · 2022Article
- Targeting GRP78 enhances the sensitivity of HOS osteosarcoma cells to pyropheophorbide-α methyl ester-mediated photodynamic therapy via the Wnt/β-catenin signaling pathway.Acta biochimica et biophysica Sinica · 2021Article
- The role of non-coding RNAs in drug resistance of oral squamous cell carcinoma and therapeutic potential.Cancer communications (London, England) · 2021Review
- Regulation of DNA methylation machinery by epi-miRNAs in human cancer: emerging new targets in cancer therapy.Cancer gene therapy · 2021Review
- miR-506 in patients with chronic myeloid leukemia and its effect on apoptosis of K562 cells.American journal of translational research · 2021Article
- Circ-PVT1/miR-106a-5p/HK2 axis regulates cell growth, metastasis and glycolytic metabolism of oral squamous cell carcinoma.Molecular and cellular biochemistry · 2020Article
- LncRNA SNHG16 Aggravates High Glucose-Induced Podocytes Injury in Diabetic Nephropathy Through Targeting miR-106a and Thereby Up-Regulating KLF9.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) play critical roles in the tumorigenesis and progression of oral squamous cell carcinoma (OSCC). MiR-106a* functions as a tumor suppressor miRNA in several cancers; however, its role in OSCC has not been elucidated. We investigated the role of miR-106a* in human OSCC and explored its relevant mechanisms. The expression of miR-106a* was significantly downregulated in OSCC tissues and cell lines. The overexpression of miR-106a* inhibited OSCC cell proliferation and the cell cycle G1-S transition, and induced apoptosis. In contrast, inhibition of miR-106a* promoted cell proliferation and G1-S transition and suppressed apoptosis. The expression of miR-106a* inversely correlated with methyl-CpG binding protein 2 (MeCP2) expression in OSCC tissues. Using a luciferase reporter assay, MeCP2 was determined to be a direct target of miR-106a*. Overexpression of miR-106a* decreased MeCP2 expression at both the mRNA and protein levels, while inhibition of miR-106a* increased MeCP2 expression. Importantly, overexpression of MeCP2 eliminated the effects of miR-106a* overexpression in OSCC cells and silencing of MeCP2 recapitulated the cellular and molecular effects observed with miR-106a* overexpression. MeCP2 may promote OSCC cell proliferation by activating the Wnt/β-Catenin signaling pathway. Taken together, our study demonstrated that miR-106a* inhibited OSCC cell proliferation by suppression of the Wnt/β-Catenin signaling pathway and induced apoptosis through regulation of Caspase 3/9 expression via targeting MeCP2. These findings suggest that miR-106a* acted as a tumor suppressor in the progression of OSCC and may be a potential new target for OSCC diagnosis and therapy.
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Identifiers
30662606PMC6291734What OpenQuestion holds
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.