ArticleJournal of cellular biochemistry2018
Silence of HDAC6 suppressed esophageal squamous cell carcinoma proliferation and migration by disrupting chaperone function of HSP90.
Article in Journal of cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 16 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.
The trial behind it
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
16 citing papers in PubMed, 28 citations in OpenAlex.
- Regulation of HDAC6 Catalytic Activity in Cancer: The Role of Post-Translational Modifications and Protein-Protein Interactions.International journal of molecular sciences · 2025Review
- Establishment of prognostic risk model and drug sensitivity based on prognostic related genes of esophageal cancer.Scientific reports · 2022Article
- Tubastatin A maintains adult skeletal muscle stem cells in a quiescent state ex vivo and improves their engraftment ability in vivo.Stem cell reports · 2022Article
- Canagliflozin, characterized as a HDAC6 inhibitor, inhibits gastric cancer metastasis.Frontiers in oncology · 2022Article
- Rictor/mTORC2 involves mitochondrial function in ES cells derived cardiomyocytes via mitochondrial Connexin 43.Acta pharmacologica Sinica · 2021Article
- Posttranslational modification and beyond: interplay between histone deacetylase 6 and heat-shock protein 90.Molecular medicine (Cambridge, Mass.) · 2021Review
- Role of HDAC6 and Its Selective Inhibitors in Gastrointestinal Cancer.Frontiers in cell and developmental biology · 2021Review
- Article
- Glucocorticoids rapidly inhibit cell migration through a novel, non-transcriptional HDAC6 pathway.Journal of cell science · 2020Article
- Epigenetic Alterations in Oesophageal Cancer: Expression and Role of the Involved Enzymes.International journal of molecular sciences · 2020Review
- Article
- Review
- HDACs control RUNX2 expression in cancer cells through redundant and cell context-dependent mechanisms.Journal of experimental & clinical cancer research : CR · 2019Article
- Concept of histone deacetylases in cancer: Reflections on esophageal carcinogenesis and treatment.World journal of gastroenterology · 2018Review
- Silence of HDAC6 suppressed esophageal squamous cell carcinoma proliferation and migration by disrupting chaperone function of HSP90.Journal of cellular biochemistry · 2018Article
- Histone deacetylase 6 expression in metastatic lymph nodes is a valuable prognostic marker for resected node-positive esophageal squamous cell cancer.Cancer management and research · 2018Article
Corrections and comments
- Retraction · 2021-12-03Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · Investigation by Journal/Publisher · Unreliable Results and/or Conclusions ·
- RetractedRetraction.2021
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal carcinoma is aggressive in nature and its prognosis is largely dependent on the degree of invasion. Histone deacetylase 6 (HDAC6), as the most unique member of HDACs family, has the positive activity to promote initiation and progression of various cancers via targeting multiple non-histone proteins in cytoplasm. In this study, we found that HDAC6 was over-expressed in three esophageal cancer cell lines (KYSE140, KYSE170, KYSE180) when compared to non-carcinoma esophageal epithelial cell HEEC-1. Then two HDAC6 specific siRNAs and HDAC6 inhibitor tubastatin A greatly suppressed KYSE140 and KYSE180 cells proliferation and migration, and the inhibition of cell motility was accompanied by elevated acetylation of α-tubulin, a target of HDAC6. Consistently, the microtubulin skeleton was stabilized after HDAC6 knockdown or inhibition. In addition, acetylation status of HSP90, another HDAC6 target, was also increased towards HDAC6 knockdown or inhibition by co-immunoprecipitation assay. Besides, co-treatment of HSP90 inhibitor (PU-H71) and HDAC6 inhibitor (tubastatin A) induced a stronger cell migration inhibition compared to administration of either drug alone. Furthermore, cell proliferation of KYSE140 and KYSE180 were also compromised in response to combination of HDAC6 and HSP90 inhibitors. Additionally, co-administration of HSP90 inhibitor and HDAC6 inhibitor strongly inhibited tumor growth in vivo. Taken together, our results indicated that HDAC6 is a promising target by inhibiting HSP90 function in ESCC.
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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.