Next Article in Journal
MicroRNAs as Diagnostic and Prognostic Biomarkers in Ischemic Stroke—A Comprehensive Review and Bioinformatic Analysis
Previous Article in Journal
Paradoxical Role of Matrix Metalloproteinases in Liver Injury and Regeneration after Sterile Acute Hepatic Failure
Article Menu
Issue 12 (December) cover image

Export Article

Open AccessArticle
Cells 2018, 7(12), 248;

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

INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, University Bourgogne Franche-Comté F-25000 Besançon, France
Department of Pathology, University Hospital of Besançon, F-25000 Besançon, France
Team Replisome Dynamics and Cancer. UMR7242 Biotechnologie et Signalisation Cellulaire, CNRS-University Strasbourg, F-67412 Illkirch, France
Ecole Supérieure de Biotechnologie de Strasbourg, University Strasbourg, CNRS, UMR 7242, F-67412 Illkirch, France
EPIGENEXP platform, University of Bourgogne Franche-Comté, F-25000 Besançon, France
Boratory of Experimental Pathology, GIGA-Cancer, University of Liege, B-4000 Liege, Belgium
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]   |  


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

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

Supplementary material


Share & Cite This Article

MDPI and ACS Style

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.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Cells EISSN 2073-4409 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top