Inhibition of histone deacetylase1 induces autophagy

• Published in: Biochemical and biophysical research communications Vol. 369; no. 4; pp. 1179 - 1183
• Main Authors: Oh, Meeyeon, Choi, In-Kwon, Kwon, Ho Jeong
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 16.05.2008
• Subjects: Animals; Antibiotics, Antineoplastic - pharmacology; Autophagy; Autophagy - drug effects; Autophagy - genetics; Depsipeptides - pharmacology; Enzyme Inhibitors - pharmacology; FK228; HeLa Cells; Histone Deacetylase 1; Histone deacetylase inhibitor; Histone Deacetylase Inhibitors; Histone deacetylase1; Histone Deacetylases - genetics; Humans; Microtubule-Associated Proteins - metabolism; RNA, Small Interfering - pharmacology; Histone deacetylase1; Histone deacetylase inhibitor; Autophagy; FK228
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2008.03.019

Autophagy is a process where cytoplasmic materials are degraded by lysosomal machinery. Histone deacetylase (HDAC) inhibitors induce autophagy, and HDAC6, one of class II HDAC isotypes, is directly involved in autophagic degradation in the cell. However, it is unclear if class I HDAC isotype such as HDCA1 is involved in this process. To investigate if class I HDAC isotype is involved in autophagy, a specific class I HDAC inhibitor and an siRNA of HDAC1 were used to treat HeLa cells. Autophagic markers were then investigated. Both inhibition and genetic knock-down of HDAC1 in the cells significantly induced autophagic vacuole formation and lysosome function. Moreover, disruption of HDAC1 leads to the conversion of LC3-I to LC3-II. Together, these results demonstrate that HDAC1 could play a role in autophagy and specific inhibition of HDAC1 can induce autophagy.