Abstract | BACKGROUND: METHODS:
Histone deacetylases7 was knocked down using HDAC7 siRNAs, and cell proliferation was quantified. Cell cycle progression, apoptosis, and autophagy were measured by flow cytometry and immunoblotting. RESULTS:
Histone deacetylases 7 siRNAs inhibited cell proliferation and c-Myc expression, increased p27 expression, and caused G2/M phase cell cycle arrest in both YD-15 and Mc3 cells. HDAC7 silencing increased the sub-G1 population, Annexin V positive apoptotic cells and cleaved caspase3 levels. HDAC7 silencing induced an increase in autophagic markers, number of acidic vesicular organelles, and LC3B II levels, and decrease in p62 levels. HDAC7 siRNAs reduced the activation of ERK. HDAC7 knockdown resulted in growth inhibition through G2/M phase cell cycle arrest and induced both apoptosis and autophagy in MEC cells. CONCLUSIONS: This study indicates that inhibition of HDAC7 might become a novel and effective therapeutic approach for treating to MEC.
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Authors | Mee-Young Ahn, Jung-Hoon Yoon |
Journal | Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
(J Oral Pathol Med)
Vol. 46
Issue 4
Pg. 276-283
(Apr 2017)
ISSN: 1600-0714 [Electronic] Denmark |
PMID | 28178760
(Publication Type: Journal Article)
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Copyright | © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. |
Chemical References |
- HDAC7 protein, human
- Histone Deacetylases
|
Topics |
- Apoptosis
- Autophagy
- Carcinoma, Mucoepidermoid
(metabolism)
- Gene Knockdown Techniques
- Gene Silencing
- Histone Deacetylases
(metabolism)
- Humans
- Salivary Gland Neoplasms
(metabolism)
|