Histone deacetylase 2 expression predicts poorer prognosis in oral cancer patients

Chang, Hao-Hueng; Chiang, Chun-Pin; Hung, Hsin-Chia; Lin, Chungwei; Deng, Yi; Kuo, Mark Yen‐Ping

doi:10.1016/j.oraloncology.2008.08.011

Cited by 105 publications

(84 citation statements)

References 29 publications

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“…HDAC2 belongs to the class I HDAC family. Studies have shown that activation and overexpression of HDAC2 are associated with many cancers, [40][41][42][43] neurodegenerative diseases, and neural toxicity. 18 In amyotrophic lateral sclerosis patients, HDAC2 levels in the motor cortex and spinal cord are elevated.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of HDAC2 Protects the Retina From Ischemic Injury

Fan

Alsarraf

Dahrouj

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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Section: Discussionmentioning

confidence: 99%

Inhibition of HDAC2 Protects the Retina From Ischemic Injury

Fan

Alsarraf

Dahrouj

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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“…They are about as a promising new class of chemotherapeutic agents. We have recently found HDAC2 overexpression in 86% of oral squamous cell carcinoma cases (12), providing a good reason for treating oral squamous cell carcinoma with HDACis. One of the HDACis, suberonylanilide hydroxamic acid, is an orally administered HDACi that has been shown to induce apoptosis in a variety of tumor cells, but the signaling pathways involved seems to be dependent on cell type and context (13)(14)(15)(16)(17)(18)(19).…”

Section: Introductionmentioning

confidence: 90%

Suberoylanilide hydroxamic acid sensitizes human oral cancer cells to TRAIL-induced apoptosis through increase DR5 expression

Yeh

Deng

Sha

et al. 2009

Molecular Cancer Therapeutics

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Suberoylanilide hydroxamic acid has been shown to selectively induce tumor apoptosis in cell cultures and animal models in several types of cancers and is about as a promising new class of chemotherapeutic agents. In addition, suberoylanilide hydroxamic acid showed synergistic anticancer activity with radiation, cisplatin, and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in some cancers. Here, we report suberoylanilide hydroxamic acid also induced apoptosis in human oral cancer cells. Western blotting showed suberoylanilide hydroxamic acid increased Fas, Fas ligand, DR4, and DR5 protein expression and activated caspase-8 and caspase-9. The apoptosis was almost completely inhibited by caspase-8 inhibitor Z-IETD-FMK and attenuated by caspase-9 inhibitor Z-LEHD-FMK. Human recombinant DR5/Fc chimera protein but not Fas/Fc or DR4/Fc significantly inhibited apoptosis induced by suberoylanilide hydroxamic acid. These results suggest that suberoylanilide hydroxamic acid induces apoptosis mainly through activation of DR5/ TRAIL death pathway. Furthermore, subtoxic concentrations of suberoylanilide hydroxamic acid sensitize two TRAIL resistant human oral cancer cells, SAS and Ca9-22, to exogenous recombinant TRAIL-induced apoptosis in a p53-independent manner. Combined treatment of suberoylanilide hydroxamic acid and TRAIL may be used as a new promising therapy for oral cancer. [Mol Cancer Ther 2009;8(9):2718-25]

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“…Increasing evidence has revealed that HDAC2 is often overexpressed in various types of tumors (10)(11)(12)(13)(14)(15). In addition, the ablation of HDAC2 markedly inhibits tumor growth and induces apoptosis (13,14,16), suggesting HDAC2 functions as oncogene in these tumors.…”

Section: Introductionmentioning

confidence: 99%

HDAC2 regulates cell proliferation, cell cycle progression and cell apoptosis in esophageal squamous cell carcinoma EC9706 cells

Wang

et al. 2016

Oncology Letters

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Abstract.Increasing evidence has demonstrated that histone deacetylase 2 (HDAC2) participates in the regulation of a variety of biological processes in numerous tumors. However, the potential role of HDAC2 in the development and progression of esophageal squamous cell carcinoma (ESCC) remains elusive. Immunohistochemistry was utilized to detect the expression of HDAC2, Cell Counting Kit-8 was used to determine the cell proliferation, and flow cytometry was employed to investigate cell cycle and cell apoptosis. Finally, western blotting was employed to detect the protein expression of cyclin D1, p21, B cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax). The present study found that expression of HDAC2 protein in ESCC tissues was significantly increased compared with atypical hyperplasia tissues and normal esophageal mucosa (P<0.001). The expression of HDAC2 was not associated with the age or gender of patients (P>0.05), but was closely associated with the histological grade, invasion depth, tumor-node-metastasis stage and lymph node metastasis, respectively (all P<0.001). HDAC2 small interfering RNA effectively downregulated the expression of HDAC2 protein in ESCC EC9706 cells. Downregulation of HDAC2 expression evidently inhibited cell proliferation, arrested cell cycle at the G0/G1 phase and induced cell apoptosis in ESCC EC9706 cells, coupled with increased expression of p21 and Bax proteins and decreased expression of cyclin D1 and Bcl-2 proteins. Overall, the present findings suggest that HDAC2 may play an important role in the development and progression of ESCC and be considered as a novel molecular target for the treatment of ESCC.

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Histone deacetylase 2 expression predicts poorer prognosis in oral cancer patients

Cited by 105 publications

References 29 publications

Inhibition of HDAC2 Protects the Retina From Ischemic Injury

Inhibition of HDAC2 Protects the Retina From Ischemic Injury

Suberoylanilide hydroxamic acid sensitizes human oral cancer cells to TRAIL-induced apoptosis through increase DR5 expression

HDAC2 regulates cell proliferation, cell cycle progression and cell apoptosis in esophageal squamous cell carcinoma EC9706 cells

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