ArticlePloS one2011
HDAC inhibition decreases the expression of EGFR in colorectal cancer cells.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed.
- Article
- Histone and non-histone protein acetylation in a tail regeneration model (Ambystoma mexicanum).Biology open · 2026Article
- Synthesis and Characterization of Sulfonamide-Schiff Bases, and Investigation of Cytotoxic, Antioxidant, HDAC, and Apoptotic Activities in Human Colon Cancer Cells (DLD-1 and HT-29).Archiv der Pharmazie · 2026Article
- Design, synthesis and molecular modeling of new coumarin-thiazole derivatives as dual EGFR/HDAC1 inhibitors:RSC advances · 2025Article
- Colorectal Cancer: Pathogenesis and Targeted Therapy.MedComm · 2025Review
- Acquired vulnerability against EGF receptor inhibition in gastric cancer promoted by class I histone deacetylase inhibitor entinostat.Neoplasia (New York, N.Y.) · 2025Article
- The influence of the microbiome on radiotherapy and DNA damage responses.Frontiers in oncology · 2025Review
- Synthesis, and biological evaluation of EGFR/HER2-NAMPT conjugates for tumor treatment.Molecular diversity · 2024Article
- Advances in targeting histone deacetylase for treatment of solid tumors.Journal of hematology & oncology · 2024Review
- Trichostatin C Synergistically Interacts with DNMT Inhibitor to Induce Antineoplastic Effect via Inhibition of Axl in Bladder and Lung Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2024Article
- SIN-3 acts in distinct complexes to regulate the germline transcriptional program in Caenorhabditis elegans.Development (Cambridge, England) · 2023Article
- Histone Deacetylases Function in the Control of Early Hematopoiesis and Erythropoiesis.International journal of molecular sciences · 2022Review
- Phospho-EGFRTyr992 is synergistically repressed by co-inhibition of histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K), which attenuates resistance to erlotinib in head and neck cancer cells.Annals of translational medicine · 2021Article
- Histone deacetylase inhibitor panobinostat induces antitumor activity in epithelioid sarcoma and rhabdoid tumor by growth factor receptor modulation.BMC cancer · 2021Article
- EGFR phosphorylates HDAC1 to regulate its expression and anti-apoptotic function.Cell death & disease · 2021Article
- HDAC inhibitors suppress the proliferation, migration and invasiveness of human head and neck squamous cell carcinoma cells via p63‑mediated tight junction molecules and p21‑mediated growth arrest.Oncology reports · 2021Article
- Histone Deacetylase Modifications by Probiotics in Colorectal Cancer.Journal of gastrointestinal cancer · 2020Review
- Amplification of a calcium channel subunit CACNG4 increases breast cancer metastasis.EBioMedicine · 2020Article
- RGFP966 Suppresses Tumor Growth and Migration Through Inhibition of EGFR Expression in Hepatocellular Carcinoma Cells in vitro.Drug design, development and therapy · 2020Article
- Trichostatin A inhibits proliferation of PC3 prostate cancer cells by disrupting the EGFR pathway.Oncology letters · 2019Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermal growth factor receptor (EGFR), a receptor tyrosine kinase which promotes cell proliferation and survival, is abnormally overexpressed in numerous tumors of epithelial origin, including colorectal cancer (CRC). EGFR monoclonal antibodies have been shown to increase the median survival and are approved for the treatment of colorectal cancer. Histone deacetylases (HDACs), frequently overexpressed in colorectal cancer and several malignancies, are another attractive targets for cancer therapy. Several inhibitors of HDACs (HDACi) are developed and exhibit powerful antitumor abilities. In this study, human colorectal cancer cells treated with HDACi exhibited reduced EGFR expression, thereby disturbed EGF-induced ERK and Akt phosphorylation. HDACi also decreased the expression of SGLT1, an active glucose transporter found to be stabilized by EGFR, and suppressed the glucose uptake of cancer cells. HDACi suppressed the transcription of EGFR and class I HDACs were proved to be involved in this event. Chromatin immunoprecipitation analysis showed that HDACi caused the dissociation of SP1, HDAC3 and CBP from EGFR promoter. Our data suggested that HDACi could serve as a single agent to block both EGFR and HDAC, and may bring more benefits to the development of CRC therapy.
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