Anti-MUC1 antibody inhibits EGF receptor signaling in cancer cells
| Autor: | Kwang Chul Kim, Hiroshi Katsuki, Ichiro Horie, Hideki Nakayama, Takeshi Miyata, Akinori Hisatsune, Yoichiro Isohama, Mitsuru Kawasaki |
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| Rok vydání: | 2011 |
| Předmět: |
Cell signaling
media_common.quotation_subject Biophysics digestive system Biochemistry Metastasis Cell Line Tumor Neoplasms Pancreatic cancer medicine Humans skin and connective tissue diseases Internalization neoplasms Molecular Biology Cell Proliferation media_common biology Chemistry Mucin-1 Antibodies Monoclonal Cancer Cell Biology medicine.disease biological factors digestive system diseases ErbB Receptors Protein Transport Cancer cell Cancer research biology.protein Signal transduction Antibody Signal Transduction |
| Zdroj: | Biochemical and Biophysical Research Communications. 405:377-381 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2011.01.029 |
| Popis: | MUC1 is a type I transmembrane glycoprotein aberrantly overexpressed in various cancer cells. High expression of MUC1 is closely associated with cancer progression and metastasis, leading to poor prognosis. We previously reported that MUC1 is internalized by the binding of the anti-MUC1 antibody, from the cell surface to the intracellular region via the macropinocytotic pathway. Since MUC1 is closely associated with ErbBs, such as EGF receptor (EGFR) in cancer cells, we examined the effect of the anti-MUC1 antibody on EGFR trafficking. Our results show that: (1) anti-MUC1 antibody GP1.4, but not another anti-MUC1 antibody C595, triggered the internalization of EGFR in pancreatic cancer cells; (2) internalization of EGFR by GP1.4 resulted in the inhibition of ERK phosphorylation by EGF stimulation, in a MUC1 dependent manner; (3) inhibition of ERK phosphorylation by GP1.4 resulted in the suppression of proliferation and migration of pancreatic cancer cells. We conclude that the internalization of EGFR by anti-MUC1 antibody GP1.4 inhibits the progression of cancer cells via the inhibition of EGFR signaling. |
| Databáze: | OpenAIRE |
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