Fiche publication
Date publication
août 2017
Journal
Scientific reports
Auteurs
Membres identifiés du Cancéropôle Est :
Dr GARBAR Christian
,
Pr MERROUCHE Yacine
,
Pr BENSUSSAN Armand
Tous les auteurs :
Garbar C, Mascaux C, Giustiniani J, Merrouche Y, Bensussan A
Lien Pubmed
Résumé
Autophagy is one of the chemotherapy resistance mechanisms in breast cancer. The aim of this study was to determine the level of recruitment of the autophagy pathway in the triple-negative breast cancer (TNBC) cell line MDA-MB231 compared with that in the control luminal breast cancer cell line MCF7 before and after treatment with chemotherapy drugs. Furthermore, we investigated the relationship between autophagy and EGFR, MUC1 and IL17-receptors as activators of autophagy. Immunohistochemistry was performed in cell culture blocks using LC3b, MUC1-C, EGFR, IL17A, IL17-RA and IL17-RB antibodies. We found that the basal autophagy level in MDA-MB231 was high, whereas it was low in MCF7. However, in contrast to MDA-MB231, the autophagy level was increased in MCF7 upon treatment with chemotherapy agents. Interestingly, we observed that the expression levels of MUC1-C, EGFR, IL17-RA, and IL17-RB were not modified by the same treatments. Furthermore, the chemotherapy treatments did not increase autophagy in TNBC cells without affecting the expression levels of MUC1-C, EGFR, IL17-RA or IL17-RB.
Mots clés
Antineoplastic Agents, pharmacology, Autophagy, drug effects, Biomarkers, Tumor, Breast Neoplasms, drug therapy, Cell Line, Tumor, Cells, Cultured, Drug Resistance, Neoplasm, drug effects, Female, Gene Expression, Humans, Immunohistochemistry, MCF-7 Cells, Triple Negative Breast Neoplasms, drug therapy
Référence
Sci Rep. 2017 Aug;7(1):7201
