Please use this identifier to cite or link to this item: https://hdl.handle.net/1822/62236

TitleKnock out of the BASIGIN/CD147 chaperone of lactate/H+ symporters disproves its pro-tumour action via extracellular matrix metalloproteases (MMPs) induction
Author(s)Marchiq, Ibtissam
Albrengues, Jean
Granja, Sara Costa
Gaggioli, Cédric
Pouysségur, Jacques
Simon, Marie-Pierre
KeywordsAnimals
Basigin
Cell Line, Tumor
Coculture Techniques
Culture Media, Conditioned
Down-Regulation
Endonucleases
Fibroblasts
Gene Expression Regulation, Neoplastic
Humans
Matrix Metalloproteinases
Mice
Monocarboxylic Acid Transporters
Muscle Proteins
Neoplasms
Paracrine Communication
Signal Transduction
Symporters
Transfection
Zinc Fingers
Gene Knockout Techniques
cancer biology
membrane transport
MCT
lactic acid
glycolysis
Issue date22-Sep-2015
PublisherImpact Journals
JournalOncotarget
CitationMarchiq, I., Albrengues, J., Granja, S., Gaggioli, C., Pouysségur, J., & Simon, M. P. (2015). Knock out of the BASIGIN/CD147 chaperone of lactate/H+ symporters disproves its pro-tumour action via extracellular matrix metalloproteases (MMPs) induction. Oncotarget, 6(28), 24636.
Abstract(s)BASIGIN/CD147/EMMPRIN is a multifunctional transmembrane glycoprotein strongly expressed in tumours. BASIGIN controls tumour metabolism, particularly glycolysis by facilitating lactic acid export through the two monocarboxylate transporters MCT1 and hypoxia-inducible MCT4. However, before being recognized as a co-carrier of MCTs, BASIGIN was described as an inducer of extracellular matrix metalloproteases (MMPs). Early on, a model emerged in which, tumour cells use the extracellular domain of BASIGIN to recognize and stimulate neighbouring fibroblasts to produce MMPs. However, this model has remained hypothetical since a direct link between BASIGIN and MMPs production has not yet been clearly established. To validate the BASIGIN/MMP hypothesis, we developed BASIGIN knockouts in three human tumour cell lines derived from glioma, colon, and lung adenocarcinoma. By using co-culture experiments of either human or mouse fibroblasts and tumour cell lines we showed, contrary to what has been abundantly published, that the disruption of BASIGIN in tumour cells and in MEFs has no action on the production of MMPs. Our findings do not support the notion that the pro-tumoural action of BASIGIN is mediated via induction of MMPs. Therefore, we propose that to date, the strongest pro-tumoural action of BASIGIN is mediated through the control of fermentative glycolysis.
TypeArticle
URIhttps://hdl.handle.net/1822/62236
DOI10.18632/oncotarget.4323
ISSN1949-2553
Publisher versionwww.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=4323&path[]=9656
Peer-Reviewedyes
AccessOpen access
Appears in Collections:ICVS - Artigos em revistas internacionais / Papers in international journals

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