EB1 Restricts Breast Cancer Cell Invadopodia Formation and Matrix Proteolysis via FAK

التفاصيل البيبلوغرافية
العنوان: EB1 Restricts Breast Cancer Cell Invadopodia Formation and Matrix Proteolysis via FAK
المؤلفون: Brice Chanez, Ali Badache, Kevin Ostacolo, Sylvie Thuault
المساهمون: Centre de Recherche en Cancérologie de Marseille (CRCM), Aix Marseille Université (AMU)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Canceropôle Provence-Alpes-Côte d’Azur (PACA), InstitutNational du Cancer, Région Sud and Site de Recherche Intégrée sur le Cancer (SIRIC), Badache, Ali
المصدر: Cells
Cells, MDPI, 2021, 10 (2), pp.388. ⟨10.3390/cells10020388⟩
Cells, 2021, 10 (2), pp.388. ⟨10.3390/cells10020388⟩
Cells, Vol 10, Iss 388, p 388 (2021)
Volume 10
Issue 2
بيانات النشر: HAL CCSD, 2021.
سنة النشر: 2021
مصطلحات موضوعية: extracellular matrix, [SDV]Life Sciences [q-bio], S. EB1 Restricts Breast Cancer Cell Invadopodia Formation and Matrix Proteolysis via breast cancer, Breast Neoplasms, macromolecular substances, Article, Metastasis, Extracellular matrix, Focal adhesion, microtubules, 03 medical and health sciences, 0302 clinical medicine, breast cancer, Transforming Growth Factor beta, Cell Line, Tumor, medicine, Humans, Gene silencing, lcsh:QH301-705.5, 030304 developmental biology, invadopodia, 0303 health sciences, FAK, Chemistry, +TIPs, General Medicine, medicine.disease, Neoplasm Proteins, Cell biology, [SDV] Life Sciences [q-bio], lcsh:Biology (General), Focal Adhesion Protein-Tyrosine Kinases, 030220 oncology & carcinogenesis, Podosomes, Proteolysis, Invadopodia, Cancer cell, Female, Microtubule-Associated Proteins, Extracellular Matrix Degradation, Proto-oncogene tyrosine-protein kinase Src
الوصف: International audience; Regulation of microtubule dynamics by plus-end tracking proteins (+TIPs) plays an essential role in cancer cell migration. However, the role of +TIPs in cancer cell invasion has been poorly addressed. Invadopodia, actin-rich protrusions specialized in extracellular matrix degradation, are essential for cancer cell invasion and metastasis, the leading cause of death in breast cancer. We, therefore, investigated the role of the End Binding protein, EB1, a major hub of the +TIP network, in invadopodia functions. EB1 silencing increased matrix degradation by breast cancer cells. This was recapitulated by depletion of two additional +TIPs and EB1 partners, APC and ACF7, but not by the knockdown of other +TIPs, such as CLASP1/2 or CLIP170. The knockdown of Focal Adhesion Kinase (FAK) was previously proposed to similarly promote invadopodia formation as a consequence of a switch of the Src kinase from focal adhesions to invadopodia. Interestingly, EB1-, APC-, or ACF7-depleted cells had decreased expression/activation of FAK. Remarkably, overexpression of wild type FAK, but not of FAK mutated to prevent Src recruitment, prevented the increased degradative activity induced by EB1 depletion. Overall, we propose that EB1 restricts invadopodia formation through the control of FAK and, consequently, the spatial regulation of Src activity.
وصف الملف: application/pdf
اللغة: English
تدمد: 2073-4409
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::443f5dd335d6356a9477bf945df97506Test
https://hal-amu.archives-ouvertes.fr/hal-03174359Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....443f5dd335d6356a9477bf945df97506
قاعدة البيانات: OpenAIRE