ArticleOncoTargets and therapy2013
RUNX3 gene promoter demethylation by 5-Aza-CdR induces apoptosis in breast cancer MCF-7 cell line.
Article in OncoTargets and therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 2 of them syntheses that pooled it.
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Who cites it
11 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.
- An early biomarker and potential therapeutic target of RUNX 3 hypermethylation in breast cancer, a system review and meta-analysis.Oncotarget · 2017Pooled it
- Clinicopathological significance and potential drug target of RUNX3 in breast cancer.Drug design, development and therapy · 2014Pooled it
- Clinical significance of determining the hypermethylation of the RUNX3 gene promoter and its cohypermethylation with the BRCA1 gene for patients with breast cancer.Journal of cancer research and clinical oncology · 2023Article
- Regulation ofCancer management and research · 2020Article
- Methylation Landscape of RUNX3 Promoter Region as a Predictive Marker for Th1/Th2 Imbalance in Bronchiolitis.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Mislocalization of Runt-related transcription factor 3 results in airway inflammation and airway hyper-responsiveness in a murine asthma model.Experimental and therapeutic medicine · 2017Article
- Truncated forms of RUNX3 Unlike Full Length Protein Alter Cell Proliferation in a TGF-β Context Dependent Manner.Iranian journal of pharmaceutical research : IJPR · 2017Article
- Low concentrations of 5-aza-2'-deoxycytidine induce breast cancer stem cell differentiation by triggering tumor suppressor gene expression.OncoTargets and therapy · 2016Article
- Methylation status of theOncology letters · 2015Article
- Baicalein increases the expression and reciprocal interplay of RUNX3 and FOXO3a through crosstalk of AMPKα and MEK/ERK1/2 signaling pathways in human non-small cell lung cancer cells.Journal of experimental & clinical cancer research : CR · 2015Article
- TES was epigenetically silenced and suppressed the epithelial-mesenchymal transition in breast cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Runt-related transcription factor 3 (RUNX3) is a tumor suppressor gene, its inactivation due to hypermethylation related to carcinogenesis. The aim of this study was to investigate the effects of 5-aza-2'-deoxycytidine (5-Aza-CdR) on cell proliferation and apoptosis by demethylation of the promoter region and restoring the expression of RUNX3 in the breast cancer MCF-7 cell line. MCF-7 cells were cultured with different concentrations (0.4-102.4 μmol/L) of 5-Aza-CdR in vitro. MTT assay was used to determine the proliferation of MCF-7 cells. Flow cytometry and Hoechst staining were used for analyzing cell apoptosis. The methylation status and expression of RUNX3 in mRNA and protein levels were measured by methylation-specific polymerase chain reaction (PCR [MSP]), reverse transcription (RT)-PCR, and Western blot. It was shown that the RUNX3 gene downregulated and hypermethylated in MCF-7 cells. 5-Aza-CdR induced demethylation, upregulated the expression of RUNX3 on both mRNA and protein levels in cancer cells, and induced growth suppression and apoptosis in vitro in a dose- and time-dependent manner. The results demonstrate that RUNX3 downregulation in breast cancer is frequently due to hypermethylation, and that 5-Aza-CdR can inhibit cell proliferation and induce apoptosis by eliminating the methylation status of RUNX3 promoter and restoring its expression.
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