ArticleJournal of experimental & clinical cancer research : CR2020
HDAC3 deteriorates colorectal cancer progression via microRNA-296-3p/TGIF1/TGFβ axis.
Article in Journal of experimental & clinical cancer research : CR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.
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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.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- CXCR2 blockade potentiates HDAC3 deletion mediated antitumor immunity in colorectal cancer.Cell death & disease · 2026Article
- Extracellular vesicles enriched with mitochondrial components from intermittently cold-exposed adipose tissue drive metabolically active adipose regeneration via miR-296-3p.Materials today. Bio · 2026Article
- Article
- Identification and verification of an eight-gene prognostic signature for colorectal cancer based on tumor-associated macrophages.BMC cancer · 2026Article
- CRISPR Screen Identifies HDAC3 as a Novel Radiosensitizing Target in Small Cell Lung Cancer.Molecular cancer therapeutics · 2026Article
- HDAC3_VS_assistant: cheminformatics-driven discovery of histone deacetylase 3 inhibitors.Molecular diversity · 2025Article
- Histone deacetylases 10 as a prognostic biomarker correlates with tumor microenvironment and therapy response in colorectal cancer.World journal of gastroenterology · 2025Article
- Unraveling the role of HDAC3 as an immunotherapy prognostic biomarker and therapeutic target in advanced non-small cell lung cancer.Respiratory research · 2025Article
- Cold atmospheric plasma drives USP49/HDAC3 axis mediated ferroptosis as a novel therapeutic strategy in endometrial cancer via reinforcing lactylation dependent p53 expression.Journal of translational medicine · 2025Article
- USP38: an important regulatory factor in tumor malignant progression.Frontiers in immunology · 2025Review
- Enterotoxigenic Bacteroides fragilis (ETBF) Enhances Colorectal Cancer Cell Proliferation and Metastasis Through HDAC3/miR-139-3p Pathway.Biochemical genetics · 2024Article
- Negative regulation of HDAC3 transcription by histone acetyltransferase TIP60 in colon cancer.Genes & genomics · 2024Article
- Endocardial HDAC3 is required for myocardial trabeculation.Nature communications · 2024Article
- Involucrasin B Inhibits the Proliferation of Caco-2 Cells by Regulating the TGFβ/SMAD2-3-4 Pathway.Molecules (Basel, Switzerland) · 2024Article
- Article
- PROTACs in Epigenetic Cancer Therapy: Current Status and Future Opportunities.Molecules (Basel, Switzerland) · 2023Review
- Chidamide and Oxaliplatin Synergistically Inhibit Colorectal Cancer Growth by Regulating the RPS27A-MDM2-P53 Axis.OncoTargets and therapy · 2023Article
- TMEM97 is transcriptionally activated by YY1 and promotes colorectal cancer progression via the GSK-3β/β-catenin signaling pathway.Human cell · 2022Article
- Identification of novel leads as potent inhibitors of HDAC3 using ligand-based pharmacophore modeling and MD simulation.Scientific reports · 2022Article
- Correction to: HDAC3 deteriorates colorectal cancer progression via microRNA-296-3p/TGIF1/TGFβ axis.Journal of experimental & clinical cancer research : CR · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundThe mechanism of histone deacetylase 3 (HDAC3) in colorectal cancer (CRC) has already been discussed. However, the feedback loop of HDAC3/microRNA (miR)-296-3p and transforming growth factor β-induced factor 1 (TGIF1) in CRC has not been explained clearly. Thus, the mainstay of this study is to delve out the mechanism of this axis in CRC.
methodsTo demonstrate that HDAC3 regulates the miR-296-3p/TGIF1/TGFβ axis and is involved in CRC progression, a series of cell biological, molecular and biochemical approaches were conducted from the clinical research level, in vitro experiments and in vivo experiments. These methods included RT-qPCR, Western blot assay, cell transfection, MTT assay, EdU assay, flow cytometry, scratch test, Transwell assay, dual luciferase reporter gene assay, chromatin immunoprecipitation, nude mouse xenograft, H&E staining and TUNEL staining.
resultsHigher HDAC3 and TGIF1 and lower miR-296-3p expression levels were found in CRC tissues. HDAC3 was negatively connected with miR-296-3p while positively correlated with TGIF1, and miR-296-3p was negatively connected with TGIF1. Depleted HDAC3 elevated miR-296-3p expression and reduced TGIF1 expression, decreased TGFβ pathway-related proteins, inhibited CRC proliferation, invasion, and migration in vitro and slowed down tumor growth and induction of apoptosis in vivo, which were reversed by miR-296-3p knockdown. Restored miR-296-3p suppressed TGIF1 and reduced TGFβ pathway-related proteins, inhibited CRC proliferation, invasion, and migration in vitro and slowed down tumor growth and induction of apoptosis in vivo, which were reversed by TGIF1 overexpression.
conclusionThis study illustrates that down-regulation of HDAC3 or TGIF1 or up-regulation of miR-296-3p discourages CRC cell progression and slows down tumor growth, which guides towards a novel direction of CRC treatment.
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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.