ErbB3-Dependent Motility and Intravasation in Breast Cancer Metastasis
| Autor: | Kun Lin Tsai, Mimi Kim, Radma Mahmood, Jeffrey E. Segall, Chengsen Xue, Magalis Vuolo, Zhong Yin Zhang, Joseph Locker, Fubo Liang, Hong Qian, Jeffrey B. Wyckoff |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Oncology
Cancer Research medicine.medical_specialty Lung Neoplasms Receptor ErbB-3 Receptor ErbB-2 Breast Neoplasms Mice SCID Biology Metastasis Mice Breast cancer Cell Movement Cell Line Tumor Internal medicine medicine Animals Humans ERBB3 Epidermal growth factor receptor skin and connective tissue diseases Mice Inbred BALB C Intravasation Mammary Neoplasms Experimental Cancer Chemotaxis Neoplastic Cells Circulating medicine.disease Primary tumor Rats Cancer research biology.protein Female |
| Zdroj: | Cancer Research. 66:1418-1426 |
| ISSN: | 1538-7445 0008-5472 |
| Popis: | A better understanding of how epidermal growth factor receptor family members (ErbBs) contribute to metastasis is important for evaluating ErbB-directed therapies. Activation of ErbB3/ErbB2 heterodimers can affect both proliferation and motility. We find that increasing ErbB3-dependent signaling in orthotopic injection models of breast cancer can enhance intravasation and lung metastasis with no effect on primary tumor growth or microvessel density. Enhanced metastatic ability due to increased expression of ErbB2 or ErbB3 correlated with stronger chemotaxis and invasion responses to heregulin β1. Suppression of ErbB3 expression reduced both intravasation and metastasis. A human breast cancer tumor tissue microarray showed a significant association between ErbB3 and ErbB2 expression and metastasis independent of tumor size. These results indicate that ErbB3-dependent signaling through ErbB3/ErbB2 heterodimers can contribute to metastasis through enhancing tumor cell invasion and intravasation in vivo and that ErbB-directed therapies may be useful for the inhibition of invasion independent of effects on tumor growth. (Cancer Res 2006; 66(3): 1418-26) |
| Databáze: | OpenAIRE |
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