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HDAC6 sustains growth stimulation by prolonging the activation of EGF receptor through the inhibition of rabaptin-5-mediated early endosome fusion in gastric cancer
- Source :
- Cancer letters. 354(1)
- Publication Year :
- 2014
-
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.
- Subjects :
- Cancer Research
Programmed cell death
Carcinogenesis
medicine.medical_treatment
Vesicular Transport Proteins
Apoptosis
Endosomes
Histone Deacetylase 6
Gene Expression Regulation, Enzymologic
Histone Deacetylases
Stomach Neoplasms
Cell Line, Tumor
medicine
Humans
Epidermal growth factor receptor
RNA, Messenger
Receptor
biology
Cell Death
Growth factor
Gene Expression Profiling
digestive, oral, and skin physiology
Cell Cycle
Cancer
Cell cycle
HDAC6
medicine.disease
Endocytosis
ErbB Receptors
Gene Expression Regulation, Neoplastic
Oncology
Cancer cell
Cancer research
biology.protein
Signal Transduction
Subjects
Details
- ISSN :
- 18727980
- Volume :
- 354
- Issue :
- 1
- Database :
- OpenAIRE
- Journal :
- Cancer letters
- Accession number :
- edsair.doi.dedup.....50cb68fb5cadbd9b183dc4c7e8849ad7