期刊
JOURNAL OF CANCER
卷 7, 期 14, 页码 2035-2044出版社
IVYSPRING INT PUBL
DOI: 10.7150/jca.15200
关键词
FAK; Pax-5; Breast cancer; EMT-MET; NF kappa B; migration; metastasis
类别
资金
- New Brunswick (NB) Innovation Foundation
- Canadian Breast Cancer Foundation-Atlantic Chapter
- Canadian Breast Cancer Society/QEII Foundation
- NB Health Research Foundation (NBHRF)
- Canadian Institutes of Health Research (CIHR) New Investigator Award
- Beatrice Hunter Cancer Research Institute (BHCRI)
- Terry Fox Strategic Health Research Training Program in Cancer Research at CIHR
- NB Health Research Foundation
- Roses of Hope Foundation (La Vie en Rose Foundation)
- Canadian Breast Cancer Foundation, Atlantic Region
- NBHRF as part of Terry Fox Strategic Health Research Training Program in Cancer Research at CIHR
- BHCRI
The study of genetic factors regulating breast cancer malignancy is a top priority to mitigate the morbidity and mortality associated with this disease. One of these factors, Pax-5, modulates cancer aggressiveness through the regulation of various components of the epithelial to mesenchymal transitioning (EMT) process. We have previously reported that Pax-5 expression profiles in cancer tissues inversely correlate with those of the Focal Adhesion Kinase (FAK), a potent activator of breast cancer malignancy. In this study, we set out to elucidate the molecular and regulatory relationship between Pax-5 and FAK in breast cancer processes. Interestingly, we found that Pax-5 mediated suppression of breast cancer cell migration is dependent of FAK activity. Our mechanistic examination revealed that Pax-5 inhibits FAK expression and activation. We also demonstrate that Pax-5 is a potent modulator of FAK repressors (p53 and miR-135b) and activator (NF kappa B) which results in the overall suppression of FAK-mediated signaling cascades. Altogether, our findings bring more insight to the molecular triggers regulating phenotypic transitioning process and signaling cascades leading to breast cancer progression.
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