ArticleOncotarget2017
Disruption of STAT3-DNMT1 interaction by SH-I-14 induces re-expression of tumor suppressor genes and inhibits growth of triple-negative breast tumor.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- STAT3 as a potential therapeutic target in triple negative breast cancer: a systematic review.Journal of experimental & clinical cancer research : CR · 2019Pooled it
- Review
- Selective disruption of DNMT1/ELK1 interactions induces DGKI re-expression and promotes temozolomide sensitivity of MGMTClinical epigenetics · 2025Article
- JAK2 Inhibition Augments the Anti-Proliferation Effects by AKT and MEK Inhibition in Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2025Article
- Uncovering a Novel Role of ROR1 in the Epigenetic Regulation of Tumor Suppressor Gene CREB3L1 in Triple-Negative Breast Cancer Cells.Biomolecules · 2025Article
- Napabucasin targets resistant triple negative breast cancer through suppressing STAT3 and mitochondrial function.Cancer chemotherapy and pharmacology · 2025Article
- Asymmetric post-translational modifications regulate the nuclear translocation of STAT3 homodimers in response to leukemia inhibitory factor.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- A review of biological targets and therapeutic approaches in the management of triple-negative breast cancer.Journal of advanced research · 2023Review
- Potentiating Therapeutic Effects of Epidermal Growth Factor Receptor Inhibition in Triple-Negative Breast Cancer.Pharmaceuticals (Basel, Switzerland) · 2021Review
- iRGD conjugated nimbolide liposomes protect against endotoxin induced acute respiratory distress syndrome.Nanomedicine : nanotechnology, biology, and medicine · 2021Article
- Comprehensive analysis of regulation of DNA methyltransferase isoforms in human breast tumors.Journal of cancer research and clinical oncology · 2021Review
- Genotoxicity and Epigenotoxicity of Carbazole-Derived Molecules on MCF-7 Breast Cancer Cells.International journal of molecular sciences · 2021Article
- Article
- Methylomic analysis identifies C11orf87 as a novel epigenetic biomarker for GI cancers.PloS one · 2021Article
- Can asymmetric post-translational modifications regulate the behavior of STAT3 homodimers?FASEB bioAdvances · 2020Article
- MPC1 deficiency accelerates lung adenocarcinoma progression through the STAT3 pathway.Cell death & disease · 2019Article
- Natural Sesquiterpene Lactones Enhance Chemosensitivity of Tumor Cells through Redox Regulation of STAT3 Signaling.Oxidative medicine and cellular longevity · 2019Review
- Combined drug therapeutic strategies for the effective treatment of Triple Negative Breast Cancer.Bioscience reports · 2018Review
- Responses to Cytokines and Interferons that Depend upon JAKs and STATs.Cold Spring Harbor perspectives in biology · 2018Review
- Inhibition of glycogen synthase kinase 3 beta (GSK3β) suppresses the progression of esophageal squamous cell carcinoma by modifying STAT3 activity.Molecular carcinogenesis · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigenetic regulation of gene expression is an emerging target to treat several human diseases including cancers. In cancers, expressions of many tumor suppressor genes are suppressed by hyper-methylation in their regulatory regions. Herein, we describe a novel carbazole SH-I-14 that decreased the level of the acetyl-STAT3 at the K685 residue. Mutation analysis revealed that SH-I-14 disrupted STAT3-DNMT1 interaction by removing acetyl group from K685 of STAT3. Finally, the inhibition of STAT3-DNMT1 interaction by SH-I-14 resulted in re-expression of tumor suppressor genes such as VHL and PDLIM4 through de-methylation of their promoter regions. In addition, SH-I-14 showed anti-proliferative effect in triple-negative breast cancer (TNBC) cell lines
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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.