Christine Varon
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Positions (1)
University of Bordeaux
University of Bordeaux
10 months ago
The University of Bordeaux, in collaboration with INSERM, ARNA, and the Bordeaux Institute of Oncology (BRIC), is offering an 18-month postdoctoral research position focused on aptamer-based nanomedicine for gastric cancer. The project, titled "Dual targeting of gastric cancer stem cells using aptamer-based nanomedicines," aims to develop innovative chemotherapy strategies targeting cancer stem cells (CSC) through aptamer nanoassemblies. The research will focus on aptamer and multivalent aptamer design, bispecific aptamer nanoassemblies, drug–aptamer conjugates, and both in vitro (2D/3D) and in vivo cancer models. Supervision will be provided by Dr. Jeanne Leblond-Chain (INSERM, ARNA) and Prof. Christine Varon (Université de Bordeaux, BRIC), with close collaboration between the ARNA research group "Targeted Aptamers, Medicines and Sensing" and BRIC Team 4 "Helicobacter-associated digestive cancers, cancer stem cells and therapeutic strategies." The project will be conducted mainly in the Bordeaux Biologie Santé building in Carreire campus, Bordeaux, France. The ideal candidate should have expertise in aptamer/nucleic acid design, synthesis, biophysics, nanomedicine, and/or biochemistry. Experience in cell culture and in vivo experiments is highly desirable. The position is suited for candidates motivated by multidisciplinary research at the chemistry–biology interface, with interests spanning nucleic acid chemistry, molecular biology, and cell biology. Applicants are required to submit a CV, grade records (Master + PhD), PhD report, motivation letter, and two reference letters to Dr. Jeanne Leblond-Chain at [email protected] by December 20th, 2025. The position is funded for 18 months, though specific financial details are not disclosed. This opportunity is ideal for postdoctoral researchers seeking to advance cancer nanomedicine and stem cell targeting in a collaborative, cutting-edge environment.
10 months ago
Articles (12)
Background The bacterial genotoxin, cytolethal distending toxin (CDT), causes DNA damage in host cells, a risk factor for carcinogenesis. Previous studies have shown that CDT induces phenotypes reminiscent of epithelial to mesenchymal transition (EMT), a process involved in cancer initiation and progression. Methods We investigated different steps of EMT in response to Helicobacter hepaticus CDT and its active CdtB subunit using in vivo and in vitro models. Results Most of the steps of the EMT process were induced by CDT/CdtB and observed throughout the study in murine and epithelial cell culture models. CdtB induced cell-cell junction disassembly, causing individualization of cells and acquisition of a spindle-like morphology. The key transcriptional regulators of EMT (SNAIL and ZEB1) and some EMT markers were upregulated at both RNA and protein levels in response to CDT/CdtB. CdtB increased the expression and proteolytic activity of matrix metalloproteinases, as well as cell migration. A range of these results were confirmed in Helicobacter hepaticus-infected and xenograft murine models. In addition, colibactin, a genotoxic metabolite produced by Escherichia coli, induced EMT-like effects in cell culture. Conclusions Overall, these data show that infection with genotoxin-producing bacteria elicits EMT process activation, supporting their role in tumorigenesis.
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2024
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2023
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2022
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2022
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2022
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2022
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2021
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2021
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2020
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2020
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2020
Collaborators (9)
Laetitia Aymeric
Associate professor
Université d'Angers
Christian Frezza
Professor of metabolomics in ageing
University of Cologne
VICTOR H. VILLAR
University of St. Andrews
Maude Everaert
Vrije Universiteit Brussel
Armelle Ménard
University of Bordeaux
Piedad-del-Socorro Murdoch
Profesora titular
Universidad de Sevilla
Raúl V. Durán
Universidad de Sevilla
Sarah Courtois
Associate Professor
Centre de Résonance Magnétique des Systèmes Biologiques
Océane Martin
Associate professor
CNRS
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