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Mevel, R.

Publications and source records attributed to Mevel, R..

3 recordsLinked to original sources

A modular patient-derived organoid-xenograft platform reveals molecular and clinical trajectories of prostate cancer progression

Patient-derived organoids (PDOs) are becoming increasingly important in prostate cancer (PCa) translational research. However, direct proof-of-concept studies demonstrating their ability to model disease evolution, identify relevant biomarkers, and accurately predict treatment response in PCa patients, remain scarce. Here, we report the establishment of serially transplantable xenografts series derived from two advanced PCa PDO lines, which can be further re-cultured as organoids. Newly-generated model series maintain key phenotypic, genomic, and functional characteristics of the original patient tumors, and emulate relevant molecular subtypes of advanced PCa. Single-cell RNA sequencing (scRNA-seq) analysis uncovers transcriptomic differences between xenograft and organoid models, as well as signaling pathways which are largely preserved and can be targeted ex vivo. Functional drug profiles correlate with molecular and clinical attributes, as exemplified by response to androgen receptor (AR) pathway inhibitors and glucocorticoid-mediated AR signaling activation. Longitudinal scRNA-seq analysis of perturbed PDOs identifies a rare PROX1+/ALDH1A1+ cell population, which pre-exist in the treatment-naive setting and is significantly enriched upon androgen deprivation. Notably, this cell population is similarly enriched in post-treatment samples of the original patient and is associated with aggressive AR-negative PCa molecular subtypes, suggesting a potential link with PCa progression. Our study provides proof-of-concept evidence that organoids can mirror PCa patient-specific drug sensitivity profiles and molecular paths of disease progression, uncovering pertinent biomarkers. Ultimately, our organoid-xenograft model series provide a modular and scalable platform that can readily be used for mechanistic and translational studies.

cancer biology↗

RUNX1 marks a luminal castration resistant lineage established at the onset of prostate development

The characterization of prostate epithelial hierarchy and lineage heterogeneity is critical to understand its regenerative properties and malignancies. Here, we report that the transcription factor RUNX1 marks a specific subpopulation of proximal luminal cells (PLCs), enriched in the periurethral region of the developing and adult mouse prostate, and distinct from the previously identified NKX3.1+ luminal castration resistant cells. Using scRNA-seq profiling and genetic lineage tracing, we show that RUNX1+ PLCs are unaffected by androgen deprivation, and do not contribute to the regeneration of the distal luminal compartments. Furthermore, we demonstrate that a transcriptionally similar RUNX1+ population emerges at the onset of embryonic prostate specification to populate the proximal region of the ducts. Collectively, our results reveal that RUNX1+ PLCs is an intrinsic castration-resistant and self-sustained lineage that emerges early during prostate development and provide new insights into the lineage relationships of the prostate epithelium.

developmental biology↗

Mesenchymal stromal cells release CXCL1/2/8 and induce chemoresistance and macrophage polarization

Factors released by surrounding cells such as cancer-associated mesenchymal stromal cells (CA-MSCs) are involved in tumor progression and chemoresistance. We determine the mechanisms by which a naive MSC could become a CA-MSC and characterize CA-MSCs. Ovarian tumor cells (OTC) trigger the transformation of MSCs to CA-MSCs expressing different pro-tumoral, genes and secreting high amounts of CXCR1/2 ligands (CXCL1, CXCL2 and IL-8) implicated in the chemoresistance of cancer cells. CXCR1/2 ligands can also inhibit the immune response against OTC. Indeed, through their released factors, CA-MSCs can trigger the differentiation of monocytes to pro-tumoral M2 phenotype macrophages known to promote the tumor progression. When CXCR1/2 receptors are inhibited, these CA-MSC-activated macrophages lose their M2 functions and acquire an anti-tumoral phenotype. Both ex vivo and in vivo a CXCR1/2 inhibitor can sensitize OTC to carboplatin even in the presence of a pro-tumoral microenvironment. This inhibitor can circumvent the pro-tumoral effects of CA-MSCs. As high concentrations of CXCR1/2 ligands in blood from patients can be associated with chemoresistance, CXCR1/2 inhibition could be a potential therapeutic strategy to revert chemoresistance.

cancer biology↗