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Elkaoutari, A.

Publications and source records attributed to Elkaoutari, A..

2 recordsLinked to original sources

Circulating colorectal tumor cells remodel their surfaceome to increase their viability and metastatic potential in the bloodstream

Circulating tumor cells (CTCs) are the potential seeds of distant metastases; however, little is known about how they survive in the bloodstream. Using a large cohort of colorectal cancer (CRC) patients, we found that the pseudokinase receptor PTK7 is highly expressed in primary tumors and metastatic lesions. Consistent with previous reports, high PTK7 expression is associated with reduced disease-free survival and increased metastatic dissemination. Surprisingly, PTK7 is absent from most CTCs and undergoes a cell-autonomous ONtumor/OFFCTC/ONmetastasis switch that can be recapitulated in a xenografted mouse model, in in vitro systems, and a fluidic platform. PTK7-negative cancer cells exhibit increased expression of YAP1-driven genes, senescence-like features, and enhanced resistance to hemodynamic stress following loss of cell-cell and cell-matrix adhesion. This adaptive phenotype depends on metalloproteases, notably ADAM17, whose cleavage activity remodels the CTCs surfaceome. Functionally, the PTK7 OFFCTC state confers enhanced metastatic potential in vivo, and can be pharmacologically suppressed using metalloprotease inhibitors. Collectively, our findings identify a reversible, cell-autonomous, protease-driven surfaceome remodeling program that enables metastatic adaptation during hematogenous dissemination. Highlights / statement of significanceBy investigating potential markers for circulating colorectal tumor cells with strong metastatic potential, we describe a reversible and cell-autonomous remodeling of the circulating tumor cell surfaceome in patients that confers resistance to anoikis and stress induced by entry into the bloodstream. One Sentence SummaryThe dynamic regulation of PTK7 serves as a surrogate marker for tumor cell plasticity, aggressiveness, survival in the bloodstream, and efficiency in forming metastases. Trial registrationCTC colon Cohort: registered on https://ClinicalTrials.gov identifier NCT03256084; date of registration 2017-07-17 B-Org cohort: registered on https://ClinicalTrials.gov NCT05384184; date of registration 2019-06-06 Ethics statement for animal experimentsStudies on animals were conducted in accordance with the current ethical standards of the European Community (Directive 2010/63/EU), the Ethics Committee for Animal Experimentation (CEEA#14) and the French Ministry of Higher Education and Research, which approved and authorized the entire procedure described in this paper (project number APAFIS #35294).

cancer biology↗

Basal-like and Classical cells coexistence in pancreatic cancer revealed by single cell analysis

Pancreatic ductal adenocarcinoma (PDAC) is composed of stromal, immune and epithelial cells. Transcriptomic analysis of the epithelial compartment allows a binary classification into mainly two phenotypic subtypes, classical and basal-like. However, little is known about the intra-tumor heterogeneity of the epithelial component. Growing evidences suggest that this two side phenotypic segregation is not so clear and that both could coexist in a single tumor. In order to elucidate this hypothesis, we performed single-cell transcriptomic analyses using combinational barcoding on epithelial cells from 6 different classical PDAC obtained by Endoscopic Ultrasound (EUS) with Fine Needle Aspiration (FNA). In order to purify the epithelial compartment, PDAC were grown as Biopsy Derived Pancreatic Cancer Organoids. Single cell transcriptomic analysis allowed the identification of 4 main cell clusters present in different proportions in all tumors. Remarkably, although these tumors were classified as Classical, one of the clusters corresponded to a basal-like. These results depict the unanticipated high heterogeneity of pancreatic cancers and demonstrated that basal-like cells with a high aggressive phenotype are more widespread than expected.

cancer biology↗