A role for EMT in CD73 regulation in breast cancer

Meriem Hasmim; Guy Berchem; Bassam Janji

doi:10.1080/2162402X.2022.2152636

A role for EMT in CD73 regulation in breast cancer

Meriem Hasmim
, Guy Berchem
, Bassam Janji^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › Research › peer-review

5 Citations (Scopus)

Abstract

CD73 is an emerging target in cancer due to its role in generating adenosine, a potent immunosuppressor. We found that SNAI1, a driver of epithelial-to-mesenchymal transition (EMT), upregulates CD73 in triple negative breast cancer cells. Here, we discuss the relevance of improving CD73-based therapy by combining with inhibitors of EMT.

Original language	English
Article number	2152636
Journal	OncoImmunology
Volume	11
Issue number	1
DOIs	https://doi.org/10.1080/2162402X.2022.2152636
Publication status	Published - 30 Nov 2022

Keywords

Humans
Epithelial-Mesenchymal Transition
Triple Negative Breast Neoplasms/genetics
Adenosine

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10.1080/2162402X.2022.2152636Licence: CC BY

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title = "A role for EMT in CD73 regulation in breast cancer",

abstract = "CD73 is an emerging target in cancer due to its role in generating adenosine, a potent immunosuppressor. We found that SNAI1, a driver of epithelial-to-mesenchymal transition (EMT), upregulates CD73 in triple negative breast cancer cells. Here, we discuss the relevance of improving CD73-based therapy by combining with inhibitors of EMT.",

keywords = "Humans, Epithelial-Mesenchymal Transition, Triple Negative Breast Neoplasms/genetics, Adenosine",

author = "Meriem Hasmim and Guy Berchem and Bassam Janji",

note = "Funding This work was supported by grants from FNRS-Televie (7.4579.20-CD73), Luxembourg National Research Fund (BRIDGES2020/BM/15412275/ SMART-COMBO; BRIDGES2021/BM/16358198/TRICK-ALDH and INTER/EUROSTARS21/16896480/C2I), Fondation Recherche Cancer et Sang, Luxembourg (INCOM BIOM), Kriibskrank Kanner Foundation; Luxembourg (Neuroimmunotherapy II-2019) and Stiftelsen Cancera (2022; Fonds De La Recherche Scientifique – FNRS). {\textcopyright} 2022 The Author(s). Published with license by Taylor \& Francis Group, LLC.",

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doi = "10.1080/2162402X.2022.2152636",

language = "English",

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AU - Hasmim, Meriem

AU - Berchem, Guy

AU - Janji, Bassam

N1 - Funding This work was supported by grants from FNRS-Televie (7.4579.20-CD73), Luxembourg National Research Fund (BRIDGES2020/BM/15412275/ SMART-COMBO; BRIDGES2021/BM/16358198/TRICK-ALDH and INTER/EUROSTARS21/16896480/C2I), Fondation Recherche Cancer et Sang, Luxembourg (INCOM BIOM), Kriibskrank Kanner Foundation; Luxembourg (Neuroimmunotherapy II-2019) and Stiftelsen Cancera (2022; Fonds De La Recherche Scientifique – FNRS). © 2022 The Author(s). Published with license by Taylor & Francis Group, LLC.

PY - 2022/11/30

Y1 - 2022/11/30

N2 - CD73 is an emerging target in cancer due to its role in generating adenosine, a potent immunosuppressor. We found that SNAI1, a driver of epithelial-to-mesenchymal transition (EMT), upregulates CD73 in triple negative breast cancer cells. Here, we discuss the relevance of improving CD73-based therapy by combining with inhibitors of EMT.

AB - CD73 is an emerging target in cancer due to its role in generating adenosine, a potent immunosuppressor. We found that SNAI1, a driver of epithelial-to-mesenchymal transition (EMT), upregulates CD73 in triple negative breast cancer cells. Here, we discuss the relevance of improving CD73-based therapy by combining with inhibitors of EMT.

KW - Humans

KW - Epithelial-Mesenchymal Transition

KW - Triple Negative Breast Neoplasms/genetics

KW - Adenosine

UR - https://pubmed.ncbi.nlm.nih.gov/36465484

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DO - 10.1080/2162402X.2022.2152636

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C2 - 36465484

SN - 2162-4011

VL - 11

JO - OncoImmunology

JF - OncoImmunology

IS - 1

M1 - 2152636

ER -

A role for EMT in CD73 regulation in breast cancer

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