ArticleOncogene2010
HDAC inhibitors regulate claudin-1 expression in colon cancer cells through modulation of mRNA stability.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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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
50 citing papers in PubMed, 120 citations in OpenAlex.
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- Modifying microbially derived short chain fatty acids to promote health.The Journal of physiology · 2026Review
- Potential risks of histone deacetylase inhibitors in cancer therapeutics and feasible combination therapeutic strategies.World journal of clinical oncology · 2025Article
- NUCKS1 promotes invasion and metastasis of colorectal cancer by stabilizing HDAC2 and activating AKT.Oncogenesis · 2025Article
- Claudins in Cancer: A Current and Future Therapeutic Target.International journal of molecular sciences · 2024Review
- The role of epigenetic modifications in Colorectal Cancer Metastasis.Clinical & experimental metastasis · 2022Review
- Microbial Metabolite Regulation of Epithelial Cell-Cell Interactions and Barrier Function.Cells · 2022Review
- Zonula occludens-1 expression is reduced in nasal epithelial cells of allergic rhinitis patients.PeerJ · 2022Article
- Resveratrol Downregulates miR-155-5p to Block the Malignant Behavior of Gastric Cancer Cells.BioMed research international · 2022Article
- Article
- Star-PAP RNA Binding Landscape Reveals Novel Role of Star-PAP in mRNA Metabolism That Requires RBM10-RNA Association.International journal of molecular sciences · 2021Article
- Dysregulated expression of claudins in cancer.Oncology letters · 2021Review
- 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
- Effect of Zebularine in Comparison to and in Combination with Trichostatin A on CIP/KIP Family (p21Cip1/Waf1/Sdi1, p27Kip1, and p57Kip2), DNMTs (DNMT1, DNMT3a, and DNMT3b), Class I HDACs (HDACs 1, 2, 3) and Class II HDACs (HDACs 4, 5, 6) Gene Expression, Cell Growth Inhibition and Apoptosis Induction in Colon Cancer LS 174T Cell Line.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Role of Claudin Proteins in Regulating Cancer Stem Cells and Chemoresistance-Potential Implication in Disease Prognosis and Therapy.International journal of molecular sciences · 2019Review
- Star-PAP controlled alternative polyadenylation coupled poly(A) tail length regulates protein expression in hypertrophic heart.Nucleic acids research · 2019Article
- Secondary Bile Acids and Short Chain Fatty Acids in the Colon: A Focus on Colonic Microbiome, Cell Proliferation, Inflammation, and Cancer.International journal of molecular sciences · 2019Review
- Review
- AU-rich element-binding proteins in colorectal cancer.World journal of gastrointestinal oncology · 2019Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Expression and cellular distribution of claudin-1, a tight junction protein, is dysregulated in colon cancer and its overexpression in colon cancer cells induced dedifferentiation and increased invasion. However, the molecular mechanism(s) underlying dysregulated claudin-1 expression in colon cancer remains poorly understood. Histone deacetylase (HDAC)-dependent histone acetylation is an important mechanism of the regulation of cancer-related genes and inhibition of HDACs induces epithelial differentiation and decreased invasion. Therefore, in this study, we examined the role of HDAC-dependent epigenetic regulation of claudin-1 in colon cancer. In this study, we show that sodium butyrate and Trichostatin A (TSA), two structurally different and widely used HDAC inhibitors, inhibited claudin-1 expression in multiple colon cancer cell lines. Further studies revealed modulation of claudin-1 mRNA stability by its 3'-UTR as the major mechanism underlying HDAC-dependent claudin-1 expression. In addition, overexpression of claudin-1 abrogated the TSA-induced inhibition of invasion in colon cancer cells suggesting functional crosstalk. Analysis of mRNA expression in colon cancer patients, showed a similar pattern of increase in claudin-1 and HDAC-2 mRNA expression throughout all stages of colon cancer. Inhibition of claudin-1 expression by HDAC-2-specific small interfering RNA further supported the role of HDAC-2 in this regulation. Taken together, we report a novel post-transcriptional regulation of claudin-1 expression in colon cancer cells and further show a functional correlation between claudin-1 expression and TSA-mediated regulation of invasion. As HDAC inhibitors are considered to be promising anticancer drugs, these new findings will have implications in both laboratory and clinical settings.
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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.