ArticleOncotarget2015
Histone demethylase RBP2 promotes malignant progression of gastric cancer through TGF-β1-(p-Smad3)-RBP2-E-cadherin-Smad3 feedback circuit.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 35 citations in OpenAlex.
- SETDB1 promotes gastric cancer progression via UPR and mTOR pathway.Cancer cell international · 2026Article
- The JMJD family histone demethylases: structure, mechanism of action, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- The resilient subset: cancer stem cells at the core of immunotherapy resistance.Immunotherapy advances · 2026Review
- RBP2 promotes gastric cancer cell migration by acting as a competitive endogenous RNA to upregulate SOX4 via sponging miR-212-3p.Scientific reports · 2025Article
- Multi-bioinformatics revealed potential biomarkers and repurposed drugs for gastric adenocarcinoma-related gastric intestinal metaplasia.NPJ systems biology and applications · 2024Article
- Review
- Review
- JMJD family proteins in cancer and inflammation.Signal transduction and targeted therapy · 2022Review
- Poly(ADP-ribose) binding and macroH2A mediate recruitment and functions of KDM5A at DNA lesions.The Journal of cell biology · 2021Article
- Prominent Role of Histone Modifications in the Regulation of Tumor Metastasis.International journal of molecular sciences · 2021Review
- The emerging role of KDM5A in human cancer.Journal of hematology & oncology · 2021Review
- Crosstalk Between Inflammatory Signaling and Methylation in Cancer.Frontiers in cell and developmental biology · 2021Review
- Mechanisms of JARID1B Up-Regulation and Its Role inFrontiers in oncology · 2021Article
- The Jumonji Domain-Containing Histone Demethylase Homolog 1D/lysine Demethylase 7A (JHDM1D/KDM7A) Is an Epigenetic Activator of RHOJ Transcription in Breast Cancer Cells.Frontiers in cell and developmental biology · 2021Article
- Elucidating the cellular response of silver nanoparticles as a potential combinatorial agent for cisplatin chemotherapy.Journal of nanobiotechnology · 2020Article
- The role and mechanism of microRNA‑18a‑5p in oral squamous cell carcinoma.Molecular medicine reports · 2019Article
- Co-activation of macrophages and T cells contribute to chronic GVHD in human IL-6 transgenic humanised mouse model.EBioMedicine · 2019Article
- Molecular alterations of cancer cell and tumour microenvironment in metastatic gastric cancer.Oncogene · 2018Review
- Insights into the Action of Inhibitor Enantiomers against Histone Lysine Demethylase 5A.Journal of medicinal chemistry · 2018Article
- MicroRNA-140 Inhibits the Epithelial-Mesenchymal Transition and Metastasis in Colorectal Cancer.Molecular therapy. Nucleic acids · 2018Article
Corrections and comments
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Authors and funding
19 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Some feedback pathways are critical in the process of tumor development or malignant progression. However the mechanisms through which these pathways are epigenetically regulated have not been fully elucidated. Here, we demonstrated that the histone demethylase RBP2 was crucial for TGF-β1-(p-Smad3)-RBP2-E-cadherin-Smad3 feedback circuit that was implicated in malignant progression of tumors and its knockdown significantly inhibited gastric cancer (GC) metastasis both in vitro and in vivo. Mechanistically, RBP2 can directly bind to E-cadherin promoter and suppress its expression, facilitating EMT and distant metastasis of GC. RBP2 can also be induced by TGF-β1, a key inducer of EMT, through phosphorylated Smad3 (p-Smad3) pathway in GC. The upregulated RBP2 can be recruited by p-smad3 to E-cadherin promoter and enhance its suppression, contributing to the promotion of metastasis of GC. In addition, the suppression of E-cadherin by RBP2 attenuated inhibition of Smad3 phosphorylation (exerted by E-cadherin), resulting further induction of RBP2 expression, and thus constituting positive feedback regulation during GC malignant progression. This TGF-β1-(p-Smad3)-RBP2-E-cadherin-Smad3 feedback circuit may be a novel mechanism for GC malignant progression and suppression of RBP2 expression may serve as a new strategy for the prevention of tumor distant metastasis.
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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.