ArticleFrontiers in oncology2021
Demethylated miR-216a Regulates High Mobility Group Box 3 Promoting Growth of Esophageal Cancer Cells Through Wnt/β-Catenin Pathway.
Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 16 citations in OpenAlex.
- HMGB3 facilitates malignant phenotype of esophageal carcinoma via histone lactylation- and Wnt/β-catenin-dependent transcription activation of c-myc.NPJ precision oncology · 2026Article
- HMGB3: A pivotal orchestrator of therapy resistance and cancer stemness in human malignancies (Review).Oncology reports · 2026Review
- TGIF2-mediated HMGB3 overexpression promotes esophageal squamous cell carcinoma proliferation and metastasis through TLR3/TGF-β signaling.Genes & diseases · 2026Article
- Shared and specific competing endogenous RNAs network mining in four digestive system tumors.Computational and structural biotechnology journal · 2024Article
- Structure and Functions of HMGB3 Protein.International journal of molecular sciences · 2024Review
- The molecular characteristics could supplement the staging system of pT2/T3N0M0 esophageal squamous cell carcinoma: a translational study based on a cohort with over 20 years of follow-up.Cancer cell international · 2024Article
- HMGB3 promotes the malignant phenotypes and stemness of epithelial ovarian cancer through the MAPK/ERK signaling pathway.Cell communication and signaling : CCS · 2023Article
- Review
- Molecular mechanisms of microRNA-216a during tumor progression.Cancer cell international · 2023Review
- Wnt signaling in colorectal cancer: pathogenic role and therapeutic target.Molecular cancer · 2022Review
- Glaucocalyxin A Inhibits the Malignant Progression of Epithelial Ovarian Cancer by Affecting the MicroRNA-374b-5p/HMGB3/Wnt-β-Catenin Pathway Axis.Frontiers in oncology · 2022Article
- Environmental Cadmium Exposure Promotes the Development, Progression and Chemoradioresistance of Esophageal Squamous Cell Carcinoma.Frontiers in cell and developmental biology · 2022Article
- Roles of HMGBs in Prognosis and Immunotherapy: A Pan-Cancer Analysis.Frontiers in genetics · 2021Article
- Pan-Cancer Analyses Reveal Oncogenic and Immunological Role of Dickkopf-1 (DKK1).Frontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEsophageal cancer (EC) is the eighth most common cause of cancer-associated mortality in humans. Recent studies have revealed the important roles of microRNAs (miRs) in mediating tumor initiation and progression. miR-216a has been found to be involved in the progression of EC, but the underlying mechanisms remain largely unknown. The aim of this study is to explore the mechanism of miR-216a and the downstream molecules in esophageal cancer. MATERIALS AND
methodsThe degree of methylation of miR-216a promoter in EC tissues and cell lines was determined with methylation specific polymerase chain reaction (MSP). The levels of miR-216a and HMGB3 in EC cells were quantified by quantitative PCR (qPCR) and Western blot (WB). EC cell lines were treated with DNA methylation inhibitor 5-aza-2'-deoxycytidine (5-AZ), miR-216a mimics, and HMGB3 siRNA to explore the effects of miR-216a and HMGB3 on the proliferation, migration, invasion, and apoptosis of cells. Dual-luciferase reporter assay was employed to verify the binding of miR-216a to the 3'UTR of HMGB2 mRNA.
resultsThe promoter of MiR-216a was hypermethylated and the expression of miR-216a was down-regulated in EC, while HMGB3 was up-regulated. Dual luciferase reporter assay confirmed the binding of miR-216a to the 3'UTR of HMGB3 mRNA. Demethylated miR-216a and miR-216a mimics elevated miR-216a expression and down-regulated HMGB3, as well as inhibited cell proliferation, migration, and invasion. Inhibiting the expression of HMGB3 played an important role in inducing apoptosis, suppressing cell expansion, and down-regulating the activity of Wnt/β-catenin pathway.
conclusionsHypermethylation in the promoter of miR-216a upregulated HMGB3 and the Wnt/β-catenin pathway, resulting in enhanced EC progression.
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