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Fromont-Hankard, G.

Publications and source records attributed to Fromont-Hankard, G..

2 recordsLinked to original sources

Single Cell Calcium profiling for the discrimination of cancer cell lines.

Calcium (Ca2+) is an essential second messenger that controls numerous cellular functions. Characteristics of intracellular Ca2+ oscillations define Ca2+ signatures representatives of the phenotype of a cell. Oncogenic functions such as migration, proliferation or resistance to chemotherapy have been associated with aberrant Ca2+ fluxes. However, the identification of Ca2+ signatures representatives of the oncogenic properties of cancer cells remains to be addressed. To characterize oncogenic Ca2+ signatures, we proposed an unbiased scalable method that combines single cell calcium imaging with unsupervised and supervised machine learning tools. Here, we applied this method to investigate the heterogeneity of Ca 2+ signatures in 16 cancer cell lines and the remodeling of oncogenic Ca2+ signatures induced by acquired docetaxel resistance and in the course of the interaction of cancer cells with fibroblasts. Finally, our method demonstrates the potential of Ca2+ profiling for discriminating cancer cells and predict their phenotypic characteristics at single cell level, and provides a framework for researchers to investigate the remodeling of the Ca2+ signature during cancer development.

cancer biology↗

Curcumin and NCLX Inhibitors Share Anti-Tumoral Mechanisms in Microsatellite-Instability-Driven Colorectal Cancer

Colorectal cancer (CRC) is associated with high mortality worldwide and new targets are needed to overcome treatment resistance. Recent evidences highlight a role of the mitochondria calcium homeostasis in the development of CRC. In this context, we aimed to evaluate the role of the mitochondrial sodium-calcium-lithium exchanger (NCLX) and its targeting in CRC. We also identified curcumin as a new potential inhibitor of NCLX. In vitro, curcumin exerted strong anti-tumoral activity through its action on NCLX with mtCa2+ and reactive oxygen species overload associated with a mitochondrial membrane depolarization, leading to reduced ATP production and apoptosis through mitochondrial permeability transition pore opening concomitant with G2/M cell cycle arrest. NCLX inhibition with either CGP37157 (a benzodiazepine derivative), small interfering RNA-mediated knock-down or knockout approaches reproduced the effects of curcumin. Altered mitochondrial respiration, cellular aerobic glycolysis and endoplasmic reticulum-mitochondria membrane perturbations participated in these mechanisms. In a xenograft mouse model, NCLX inhibitors decreased CRC tumor growth. Both transcriptomic analysis of The Cancer Genome Atlas dataset and immunohistochemical analysis of tissue microarrays from 381 patients with microsatellite instability (MSI)-driven CRC demonstrated that higher NCLX expression was associated with MSI status and for the first time NCLX expression was significantly associated with recurrence-free survival in MSI CRC patients. Our findings provide strong evidence that blocking NCLX inhibits CRC in vitro and in vivo. We highlight a novel anti-tumoral mechanism of curcumin through its action on NCLX and mitochondria calcium overload that could benefit for therapeutic treatment of patients with MSI CRC.

cancer biology↗