| Literature DB >> 25111897 |
Se Jin Park1, Jeong Kyu Kim1, Hyun Jin Bae1, Jung Woo Eun1, Qingyu Shen1, Hyung Seok Kim1, Woo Chan Shin1, Hee Doo Yang1, Eun Kyung Lee2, Jueng Soo You3, Won Sang Park1, Jung Young Lee1, Suk Woo Nam4.
Abstract
The aberrant regulation of histone deacetylase 6 (HDAC6) contributes to malignant progression in various types of cancer, but the mechanism underlying gastric carcinogenesis remains unknown. Aberrant HDAC6 overexpression was observed in a subset of human gastric cancer cells. HDAC6 knockdown caused the significant inhibition of gastric cancer cell growth without affecting the transition of cell cycles or the processing of cell death. We demonstrate that an increase in epidermal growth factor receptor (EGFR) signaling through decreased EGFR degradation was mediated by HDAC6 in gastric carcinogenesis. These results establish a molecular mechanism responsible for oncogenic HDAC6, explaining how EGFR signaling induced by the growth factor is sustained during the malignant progression of gastric cancer.Entities:
Keywords: EGF receptor; Endocytosis; Histone deacetylase 6; Rabaptin-5
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Year: 2014 PMID： 25111897 DOI： 10.1016/j.canlet.2014.07.041
Source DB: PubMed Journal: Cancer Lett ISSN： 0304-3835 Impact factor: 8.679