L’invasion des cellules tumorales

Albrengues, Jean; Meneguzzi, Guerríno; Gaggioli, Cédric

doi:10.1051/medsci/20143004012

Cited by 17 publications

(9 citation statements)

References 30 publications

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“…S3 ). Because recent studies have highlighted the importance of JAK1 in tumor cell invasion ( Sanz-Moreno et al, 2011 ; Albrengues et al, 2014 ; Orgaz et al, 2014 ) and the role of IQGAP1 in matrix remodeling ( Sakurai-Yageta et al, 2008 ), we focused on these binding partners.…”

Section: Resultsmentioning

confidence: 99%

Roles of paxillin family members in adhesion and ECM degradation coupling at invadosomes

Petropoulos

Oddou

Emadali

et al. 2016

Journal of Cell Biology

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Section: Resultsmentioning

confidence: 99%

Roles of paxillin family members in adhesion and ECM degradation coupling at invadosomes

Petropoulos

Oddou

Emadali

et al. 2016

Journal of Cell Biology

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“…It is well known that when in contact with tumour cells, fibroblasts can acquire a specific CAF activated phenotype. This can result in the expression of new markers, such as alpha smooth muscle actin (α-SMA), the activation of TGFβ/SMAD signalling pathways and acquisition of new properties, such as matrix remodelling [ 24 , 25 ]. We thus, tested if conditioned media from LS174T and U87 tumour cells are able to activate stimulated NHF in vitro .…”

Section: Resultsmentioning

confidence: 99%

“…MMP activity was detected using zymogel technology [ 24 ]. Gelatin zymogels were performed as follows.…”

Section: Methodsmentioning

confidence: 99%

“…Around cancer cells, most of the fibroblasts acquire an activated status, and are known as carcinoma associated fibroblasts (CAF). The presence of CAFs is often associated with bad clinical prognosis, and a number of recent studies indicate that CAFs could play an important role in all steps of tumour progression, from initiation until metastasis [ 24 – 26 ]. Therefore, the notion that BASIGIN could serve as an inducer of MMPs is an attractive and interesting hypothesis in the context of tumour microenvironment and metastasis.…”

Section: Introductionmentioning

confidence: 99%

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Knock out of the BASIGIN/CD147 chaperone of lactate/H+ symporters disproves its pro-tumour actionviaextracellular matrix metalloproteases (MMPs) induction

et al. 2015

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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.

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“…As shown in Fig. 2 , possible drivers are stimulatory factors that are secreted by tumor cells during carcinoma development 81 . By using a 3-dimensional (3D) collagen matrix, Anderson and his collaborators showed that chemical factors secreted by melanoma cells induced fibroblasts to migrate toward, surround, and then infiltrate the tumor mass.…”

Section: Introductionmentioning

confidence: 99%

Perspective of Targeting Cancer-Associated Fibroblasts in Melanoma

Zhou¹,

Yang²,

Andl³

et al. 2015

J. Cancer

100

110

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Melanoma is known as an exceptionally aggressive and treatment-resistant human cancer. Although a great deal of progress has been made in the past decade, including the development of immunotherapy using immune checkpoint inhibitors and targeted therapy using BRAF, MEK or KIT inhibitors, treatment for unresectable stage III, stage IV, and recurrent melanoma is still challenging with limited response rate, severe side effects and poor prognosis, highlighting an urgent need for discovering and designing more effective approaches to conquer melanoma. Melanoma is not only driven by malignant melanocytes, but also by the altered communication between neoplastic cells and non-malignant cell populations, including fibroblasts, endothelial and inflammatory cells, in the tumor stroma. Infiltrated and surrounding fibroblasts, also known as cancer-associated fibroblasts (CAFs), exhibit both phenotypical and physiological differences compared to normal dermal fibroblasts. They acquire properties of myofibroblasts, remodel the extracellular matrix (ECM) and architecture of the diseased tissue and secrete chemical factors, which all together promote the transformation process by encouraging tumor growth, angiogenesis, inflammation and metastasis and contribute to drug resistance. A number of in vitro and in vivo experiments have shown that stromal fibroblasts promote melanoma cell proliferation and they have been targeted to suppress tumor growth effectively. Evidently, a combination therapy co-targeting tumor cells and stromal fibroblasts may provide promising strategies to improve therapeutic outcomes and overcome treatment resistance. A significant benefit of targeting CAFs is that the approach aims to create a tumor-resistant environment that inhibits growth of melanomas carrying different genetic mutations. However, the origin of CAFs and precise mechanisms by which CAFs contribute to melanoma progression and drug resistance remain poorly understood. In this review, we discuss the origin, activation and heterogeneity of CAFs in the melanoma tumor microenvironment and examine the contributions of stromal fibroblasts at different stages of melanoma development. We also highlight the recent progression in dissecting and characterizing how local fibroblasts become reprogrammed and build a dynamic yet optimal microenvironment for tumors to develop and metastasize. In addition, we review key developments in ongoing preclinical studies and clinical applications targeting CAFs and tumor-stroma interactions for melanoma treatment.

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L’invasion des cellules tumorales

Cited by 17 publications

References 30 publications

Roles of paxillin family members in adhesion and ECM degradation coupling at invadosomes

Roles of paxillin family members in adhesion and ECM degradation coupling at invadosomes

Knock out of the BASIGIN/CD147 chaperone of lactate/H+ symporters disproves its pro-tumour actionviaextracellular matrix metalloproteases (MMPs) induction

Perspective of Targeting Cancer-Associated Fibroblasts in Melanoma

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