| First Author | Schackmann RC | Year | 2013 |
| Journal | Cancer Res | Volume | 73 |
| Issue | 15 | Pages | 4937-49 |
| PubMed ID | 23733751 | Mgi Jnum | J:199571 |
| Mgi Id | MGI:5503241 | Doi | 10.1158/0008-5472.CAN-13-0180 |
| Citation | Schackmann RC, et al. (2013) Loss of p120-Catenin Induces Metastatic Progression of Breast Cancer by Inducing Anoikis Resistance and Augmenting Growth Factor Receptor Signaling. Cancer Res 73(15):4937-49 |
| abstractText | Metastatic breast cancer remains the chief cause of cancer-related death among women in the Western world. Although loss of cell-cell adhesion is key to breast cancer progression, little is known about the underlying mechanisms that drive tumor invasion and metastasis. Here, we show that somatic loss of p120-catenin (p120) in a conditional mouse model of noninvasive mammary carcinoma results in formation of stromal-dense tumors that resemble human metaplastic breast cancer and metastasize to lungs and lymph nodes. Loss of p120 in anchorage-dependent breast cancer cell lines strongly promoted anoikis resistance through hypersensitization of growth factor receptor (GFR) signaling. Interestingly, p120 deletion also induced secretion of inflammatory cytokines, a feature that likely underlies the formation of the prometastatic microenvironment in p120-negative mammary carcinomas. Our results establish a preclinical platform to develop tailored intervention regimens that target GFR signals to treat p120-negative metastatic breast cancers. Cancer Res; 73(15); 4937-49. (c)2013 AACR. |
