Inhibition of histone deacetylase1 induces autophagy

Oh, Meeyeon; Choi, In Kwon; Kwon, Ho Jeong

doi:10.1016/j.bbrc.2008.03.019

Cited by 92 publications

(70 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…38 SAHA, a potent HDAC inhibitor, is currently under evaluation in clinical trials. 39 SAHA-induced autophagy is reported in several cancer cell lines, 26,27 however, relatively little is known about autophagic responses in SAHA-treated leukemia cells. In this DNA, protein and lipid from oxidized damage, protecting cells from ROS-induced cell death.…”

Section: Discussionmentioning

confidence: 99%

“…21,22 Anticancer effects of SAHA are linked to the induction of apoptosis, growth arrest, polyploidy and autophagy. [23][24][25] Previous studies demonstrate that SAHA and other HDACi could induce autophagy in diverse transformed and cancer cell lines, 26,27 but the underlying mechanism of SAHA-induced autophagy is largely unknown.…”

Section: Proteomic Analysis Revealed Association Of Aberrant Ros Signmentioning

confidence: 99%

See 1 more Smart Citation

Proteomic analysis revealed association of aberrant ROS signaling with suberoylanilide hydroxamic acid-induced autophagy in Jurkat T-leukemia cells

Li¹,

Li²,

Y³

et al. 2010

Autophagy

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Proteomic Analysis Revealed Association Of Aberrant Ros Signmentioning

confidence: 99%

Proteomic analysis revealed association of aberrant ROS signaling with suberoylanilide hydroxamic acid-induced autophagy in Jurkat T-leukemia cells

Li¹,

Li²,

Y³

et al. 2010

Autophagy

View full text Add to dashboard Cite

show abstract

“…We hypothesize that lithium affects the degradation of mutant huntingtin in two ways: through the down-regulation of HDAC1 and through the induction of autophagy. Inhibition of HDACs not only induces autophagy (72)(73)(74) but also increases acetylation and enhances the clearance of mutant huntingtin. These results provide an explanation for the similar clinical efficacy of lithium and VPA and also confirm the crucial role of HDAC1 in neurodegenerative diseases.…”

Section: Discussionmentioning

confidence: 99%

Lithium Down-regulates Histone Deacetylase 1 (HDAC1) and Induces Degradation of Mutant Huntingtin

Zheng

Huang

et al. 2013

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Lithium and valproic acid (VPA) exhibit a robust neuroprotective and anti-tumor effects in neural cells and tumor cells. Results: Lithium significantly down-regulates HDAC1 at the translational level by targeting HDAC1 mRNA. Conclusion:The decrease in HDAC1 is essential for the lithium-mediated, autophagic degradation of mutant huntingtin. Significance: This report is the first demonstration that HDAC1 decreases in response to lithium treatment.

show abstract

“…One possible mechanism of non-apoptotic cell death induced by HDAC inhibitors is induction of autophagy. For example, FK228, an HDAC class I inhibitor and HDAC1 siRNA induce autophagy in HeLa cells in vitro 50 . SAHA caused tumor growth slowdown of glioblastoma xenografts in mice in which it induced autophagy.…”

Section: Histone Deacetylase Inhibitors and Apoptosismentioning

confidence: 99%

Histone deacetylase inhibitors in cancer therapy. A review

Hraběta¹,

Stiborová²,

Adam³

et al. 2014

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

View full text Add to dashboard Cite

a Background. Despite recent success toward discovery of more effective anticancer drugs, chemoresistance remains a major cause of treatment failure. There is emerging evidence that epigenetics plays a key role in the development of the resistance. Epigenetic regulators such as histone acetyltransferases (HATs) and histone deacetylases (HDACs) play an important role in gene expression. The latter are found to be commonly linked with many types of cancers and influence cancer development. Overall, histone acetylation is being investigated as a therapeutic target because of its importance in regulating gene expression. This review summarizes mechanisms of the anticancer effects of histone deacetylase (HDAC) inhibitors and the results of clinical studies. Results. Different HDAC inhibitors induce cancer cell death by different mechanisms that include changes in gene expression and alteration of both histone and non-histone proteins. Enhanced histone acetylation in tumors results in modification of expression of genes involved in cell signaling. Inhibition of HDACs causes changed expression in 2-10 % of genes involved in important biological processes. The results of experiments and clinical studies demonstrate that combination of HDAC inhibitors with some anticancer drugs have synergistic or additive effects. Conclusions. Even though many biological effects of HDAC inhibitors have been found, most of the mechanisms of their action remain unclear. In addition, their use in combination with other drugs and the combination regime need to be investigated. The discovery of predictive factors is also necessary. Finally, a key question is whether the pan-HDAC inhibitors or the selective inhibitors will be more efficient for different types of cancers.

show abstract

Inhibition of histone deacetylase1 induces autophagy

Cited by 92 publications

References 21 publications

Proteomic analysis revealed association of aberrant ROS signaling with suberoylanilide hydroxamic acid-induced autophagy in Jurkat T-leukemia cells

Proteomic analysis revealed association of aberrant ROS signaling with suberoylanilide hydroxamic acid-induced autophagy in Jurkat T-leukemia cells

Lithium Down-regulates Histone Deacetylase 1 (HDAC1) and Induces Degradation of Mutant Huntingtin

Histone deacetylase inhibitors in cancer therapy. A review

Contact Info

Product

Resources

About