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Cells 2018, 7(12), 248; https://doi.org/10.3390/cells7120248

ATG9A Is Overexpressed in Triple Negative Breast Cancer and Its In Vitro Extinction Leads to the Inhibition of Pro-Cancer Phenotypes

1
INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, University Bourgogne Franche-Comté F-25000 Besançon, France
2
Department of Pathology, University Hospital of Besançon, F-25000 Besançon, France
3
Team Replisome Dynamics and Cancer. UMR7242 Biotechnologie et Signalisation Cellulaire, CNRS-University Strasbourg, F-67412 Illkirch, France
4
Ecole Supérieure de Biotechnologie de Strasbourg, University Strasbourg, CNRS, UMR 7242, F-67412 Illkirch, France
5
EPIGENEXP platform, University of Bourgogne Franche-Comté, F-25000 Besançon, France
6
Boratory of Experimental Pathology, GIGA-Cancer, University of Liege, B-4000 Liege, Belgium
7
DimaCell platform, Univ. Bourgogne Franche-Comté, F-25000 Besançon, France
*
Author to whom correspondence should be addressed.
Received: 21 September 2018 / Revised: 26 November 2018 / Accepted: 29 November 2018 / Published: 6 December 2018
(This article belongs to the Section Autophagy)
Full-Text   |   PDF [2022 KB, uploaded 6 December 2018]   |  

Abstract

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 (ATG9A, ATG9B, BECLIN1, LC3B, NIX and P62/SQSTM1) in breast cancer tissue, and compared their expression with healthy adjacent tissue. In our study, we observed an increase in ATG9A 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 ATG9A 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 ATG9A 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. View Full-Text
Keywords: ATG9A; autophagy; triple negative breast cancer; MDA-MB-436; shRNA; CRISPR/Cas9 ATG9A; autophagy; triple negative breast cancer; MDA-MB-436; shRNA; CRISPR/Cas9
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Claude-Taupin, A.; Fonderflick, L.; Gauthier, T.; Mansi, L.; Pallandre, J.-R.; Borg, C.; Perez, V.; Monnien, F.; Algros, M.-P.; Vigneron, M.; Adami, P.; Delage-Mourroux, R.; Peixoto, P.; Herfs, M.; Boyer-Guittaut, M.; Hervouet, E. ATG9A Is Overexpressed in Triple Negative Breast Cancer and Its In Vitro Extinction Leads to the Inhibition of Pro-Cancer Phenotypes. Cells 2018, 7, 248.

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