Is Overexpressed in Triple Negative Breast Cancer and Its In Vitro Extinction Leads to the Inhibition of Pro-Cancer Phenotypes.

Fiche publication

Date publication

décembre 2018

Journal

Cells

Auteurs

Membres identifiés du Cancéropôle Est :
Dr ADAMI Pascale , Pr BORG Christophe , Pr GUITTAUT Michaël , Pr DELAGE-MOURROUX Régis , Mr MONNIEN Franck , Dr HERVOUET Eric , Dr PEIXOTO Paul , Dr MANSI Laura

Tous les auteurs :
Claude-Taupin A, Fonderflick L, Gauthier T, Mansi L, Pallandre JR, Borg C, Perez V, Monnien F, Algros MP, Vigneron M, Adami P, Delage-Mourroux R, Peixoto P, Herfs M, Boyer-Guittaut M, Hervouet E

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/30563263

Résumé

Early detection and targeted treatments have led to a significant decrease in mortality linked to breast cancer (BC), however, important issues need to be addressed in the future. One of them will be to find new triple negative breast cancer (TNBC) therapeutic strategies, since none are currently efficiently targeting this subtype of BC. Since numerous studies have reported the possibility of targeting the autophagy pathway to treat or limit cancer progression, we analyzed the expression of six autophagy genes (, , , , and ) in breast cancer tissue, and compared their expression with healthy adjacent tissue. In our study, we observed an increase in mRNA expression in TNBC samples from our breast cancer cohort. We also showed that this increase of the transcript was confirmed at the protein level on paraffin-embedded tissues. To corroborate these in vivo data, we designed shRNA- and CRISPR/Cas9-driven inhibition of expression in the triple negative breast cancer cell line MDA-MB-436, in order to determine its role in the regulation of cancer phenotypes. We found that inhibition led to an inhibition of in vitro cancer features, suggesting that ATG9A can be considered as a new marker of TNBC and might be considered in the future as a target to develop new specific TNBC therapies.