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Lerondel, S.

Publications and source records attributed to Lerondel, S..

3 recordsLinked to original sources

Forecasting tumor growth kinetics and hypoxia levels in mice using mathematical modelling

Quantitative description of tumor growth is challenged by vascular heterogeneity and hypoxia. In this study, mammary tumor growth was investigated in mouse model using caliper and ultrasound imaging measurements, bioluminescence imaging (BLI), and pimonidazole imaging. Tumor volume increased monotonically when assessed by caliper and ultrasound imaging, whereas BLI exhibited oscillating dynamics despite continued tumor growth, consistent with hypoxia-related signal attenuation. A mathematical compartmental model was developed primarily to describe tumor growth dynamics, incorporating latent vascular capacity as a key regulatory variable. The model accounts for reciprocal interactions between tumor expansion and vascular limitation. BLI was integrated as an auxiliary observable to reveal hypoxia-driven modulation of signal production rather than as a direct surrogate of tumor size. Model parameters were estimated using nonlinear mixed-effects modelling with population approach, allowing quantification of population-level behavior and inter-individual variability. The model adequately described tumor growth while explaining BLI dynamics through vascular and hypoxic effects. This framework provides the first semi-mechanistic description of tumor growth and supports the use of BLI as an indirect marker of hypoxia and, consequently, of tumor growth. This model may provide a useful framework for quantifying the effects of vascular-modulating therapeutics and genetic polymorphisms involved in tumor progression.

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↗

Malignant assignment of neuronal Na+ leak channel, NALCN: governor of Ca2+ oscillations-encoded invadopodogenesis

Cytosolic Ca2+ oscillations provide signaling input to several effector systems of the cell. These include neuronal development, migration and networking. Although similar signaling events are hijacked by highly aggressive cancer cells, the complexity of the neuron-like remodeling in metastasis remains to be explored. Here, using a variety of in vitro and in vivo techniques we show that strongly metastatic prostate cancer cells acquire specific Na+/Ca2+ signature required for persistent invasion. We identify the neuronal Na+ leak channel, NALCN, at the hot spots of the Ca2+ wave initiation and invadopodia formation. Mechanistically, NALCN associates functionally with plasmalemmal and mitochondrial Na+/Ca2+ exchangers, reactive oxygen species and store-operated channels to generate intracellular Ca2+ oscillations. In turn, this stimulates the activity of protooncogene Src kinase co-localized with NALCN, actin remodeling and secretion of proteolytic enzymes, thus increasing an invasive potential of the cancer cells and metastatic lesions in vivo (accessed in pre-clinical models). Overall, our findings provide new insight into the signaling pathway specific for metastatic cells where NALCN plays the role of the persistent invasion "launcher and controller".

cell biology↗