Dual inhibition of EGFR at protein and activity level via combinatorial blocking of PI4KIIα as anti-tumor strategy

Our previous studies indicate that phosphatidylinositol 4-kinase IIα can promote the growth of multi-malignant tumors viaHER-2/PI3K andMAPK pathways.However, the molecular mechanisms of this pathway and its potential for clinical application remain unknown. In this study, we found that PI4KIIα could...

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Bibliographic Details
Published in:Protein & cell 2014-06, Vol.5 (6), p.457-468
Main Authors: Li, Jiangmei, Zhang, Lunfeng, Gao, Zhen, Kang, Hua, Rong, Guohua, Zhang, Xu, Chen, Chang
Format: Article
Language:English
Subjects:
Animals
Antineoplastic Agents - pharmacology
Biochemistry
Biomedical and Life Sciences
breast cancer
Breast Neoplasms - metabolism
Breast Neoplasms - pathology
Cell Biology
Cell Line, Tumor
Cell Survival - drug effects
Developmental Biology
dual inhibition
EGFR
enhanced anti-tumor effect
Female
HSP90 Heat-Shock Proteins - metabolism
Human Genetics
Humans
Iressa
Life Sciences
Male
MCF-7 Cells
Mice
Mice, Inbred BALB C
Mice, Nude
Minor Histocompatibility Antigens
Mitogen-Activated Protein Kinases - metabolism
Phosphatidylinositol 3-Kinases - metabolism
phosphatidylinositol 4-kinase IIα (PI4KIIα)
Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors
Phosphotransferases (Alcohol Group Acceptor) - genetics
Phosphotransferases (Alcohol Group Acceptor) - metabolism
Protein Science
Proto-Oncogene Proteins c-akt - metabolism
Quinazolines - pharmacology
Receptor, Epidermal Growth Factor - antagonists & inhibitors
Receptor, Epidermal Growth Factor - metabolism
Research Article
Stem Cells
Transplantation, Heterologous
Tyrphostins - pharmacology
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Summary:Our previous studies indicate that phosphatidylinositol 4-kinase IIα can promote the growth of multi-malignant tumors viaHER-2/PI3K andMAPK pathways.However, the molecular mechanisms of this pathway and its potential for clinical application remain unknown. In this study, we found that PI4KIIα could be an ideal combinatorial target for EGFR treatment via regulating EGFR degradation. Results showed that PI4KIIα knockdown reduced EGFR protein level, and the expression ofPI4KIIα shows a strong correlation with EGFR in human breast cancer tissues ( r = 0.77, P
ISSN:1674-800X
1674-8018
DOI:10.1007/s13238-014-0055-y