ArticleOncotarget2017
Methylation decreases the Bin1 tumor suppressor in ESCC and restoration by decitabine inhibits the epithelial mesenchymal transition.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Aberrant DNA Methylation in Esophageal Squamous Cell Carcinoma and its Clinical Implications in Systemic Chemotherapy.International journal of medical sciences · 2025Review
- Mechanisms of radiotherapy resistance and radiosensitization strategies for esophageal squamous cell carcinoma.Molecular cancer · 2023Review
- BIN1 in cancer: biomarker and therapeutic target.Journal of cancer research and clinical oncology · 2023Review
- Pre-Clinical Evaluation of the Hypomethylating Agent Decitabine for the Treatment of T-Cell Lymphoblastic Lymphoma.Cancers · 2023Article
- Bridging Integrator 3 (BIN3) Downregulation Predicts a Poor Prognosis in Patients with Esophagus Carcinoma: A Study based on TCGA Data.Combinatorial chemistry & high throughput screening · 2023Article
- The Prognostic Significance of theIndian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2022Article
- Long non-coding RNA SNHG10 upregulates BIN1 to suppress the tumorigenesis and epithelial-mesenchymal transition of epithelial ovarian cancer via sponging miR-200a-3p.Cell death discovery · 2022Article
- Review
- Review
- Aberrant DNA Methylation in Esophageal Squamous Cell Carcinoma: Biological and Clinical Implications.Frontiers in oncology · 2020Review
- Reactivation of oncogenes involved in G1/S transcription and apoptosis pathways by low dose decitabine promotes HT29 human colon cancer cell growth in vitro.American journal of translational research · 2020Article
- DNA Methylation Status in Cancer Disease: Modulations by Plant-Derived Natural Compounds and Dietary Interventions.Biomolecules · 2019Review
- CDK5 neutralizes the tumor suppressing effect of BIN1 via mediating phosphorylation of c-MYC at Ser-62 site in NSCLC.Cancer cell international · 2019Article
- Drugs Targeting Epigenetic Modifications and Plausible Therapeutic Strategies Against Colorectal Cancer.Frontiers in pharmacology · 2019Review
- Genomic and Epigenomic Aberrations in Esophageal Squamous Cell Carcinoma and Implications for Patients.Gastroenterology · 2018Review
- DNA methylation affects metastasis of renal cancer and is associated with TGF-β/RUNX3 inhibition.Cancer cell international · 2018Article
- BIN1 reverses PD-L1-mediated immune escape by inactivating the c-MYC and EGFR/MAPK signaling pathways in non-small cell lung cancer.Oncogene · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bridging integrator-1 (Bin1), as a tumor suppressor, is frequently attenuated or even abolished in multiple primary cancers. A reduced expression of Bin1 caused by DNA methylation, has been reported in breast and prostate cancers. However, the methylation status of Bin1 and potent biological functions in esophageal squamous cell carcinoma (ESCC) remain unclear. In a previous study, we showed that the Bin1 expression was low in ESCC tissues. Herein, we further characterized this mechanism, confirming that gene hypermethylation was significantly correlated with the aberrant attenuation of Bin1. In addition, the Bin1 hypermethylation was associated with the poorer clinical parameters and shorter survival times of ESCC patients. Methylation-specific reverse transcription-polymerase chain reaction (MS-RT-PCR) showed that Bin1 was hypermethylated in several ESCC cell lines, which might be the main cause of reduced Bin1 expression. In addition, treatment with the de-methylation agent Decitabine (DAC) could restore Bin1 expression and evidently restrained ESCC cell malignant behaviors, particularly the epithelial mesenchymal transition (EMT) via reactivating the PTEN/AKT signaling pathway to inhibit matrix metalloproteinase (MMP)-2 and MMP-9 expression in vitro and in vivo. In conclusion, these results demonstrated that Bin1 methylation could augment the malignant biological behaviors of ESCC and predict the poor prognosis for ESCC patients, thus indicating the potential clinical application value of DAC-based de-methylation therapy in ESCC.
Indexed as
Identifiers
What 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.