In Vivo Isolation Of A Quiescent Melanoma Population With Invasive Properties Unveils A Transcriptional Reprogramming Driven By The Tumor Niche
Lanfrancone, L.; Lotti, F.; Meliksetyan, M.; Malferrari, M.; Quaresima, N.; Rapino, S.; Mollo, V.; Ferrarotto, I.; Vlachou, T.; Bossi, D.; Pelicci, P. G.; Luzi, L.
Show abstract
Melanoma is a heterogeneous tumor composed of many interacting cellular populations and highly plastic melanoma cells that pass through distinct cell states to adapt to the surrounding microenvironment. Slow cycling is a transient state that defines a minor population of cells with cancer-initiating features. These cells are enriched upon drug therapy and can trigger cancer relapse and metastasis dissemination when they acquire proliferative potential. This population is still not entirely characterized. Here we provide evidence of the existence of a slow cycling melanoma population isolated in vivo from melanoma PDXs using the H2B-GFP system. These cells display a highly invasive phenotype and are able to dynamically respond to cancer microenvironmental stimuli. Single cell transcriptomic analysis unveils a significant transcriptional heterogeneity of GFP-retaining slow cycling cells, defining a quiescent subpopulation of cells. These cells show a different phenotype in primary tumors and matched metastases, suggesting that tumor niche pressure drives a transcriptional reprogramming of quiescent cells during melanoma progression.
Matching journals
The top 9 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Targeting the dependence on PIK3C3-mTORC1 signaling in dormancy-prone breast cancer cells blunts metastasis initiation 96%
- BRAF inhibitors reprogram cancer-associated fibroblasts to drive matrix remodeling and therapeutic escape in melanoma 95%
- Spatiotemporal profiling defines persistence and resistance dynamics during targeted treatment of melanoma 95%
Similar papers in this journal
- ZEB1 controls a lineage-specific transcriptional program essential for melanoma cell state transitions 97%
- FRA1 drives melanoma metastasis through an actionable transcriptional network 96%
- Inhibition of the YAP-MMB interaction and targeting NEK2 as potential therapeutic strategies for YAP-driven cancers 95%
Similar papers in this journal
- Anti-CSF-1R therapy with combined immuno- chemotherapy coordinate an adaptive immune response to eliminate macrophage enriched Triple Negative Breast Cancers 96%
- Melanoblast transcriptome analysis reveals novel pathways promoting melanoma metastasis 96%
- Primary tumor associated macrophages activate programs of invasion and dormancy in disseminating tumor cells. 96%
Similar papers in this journal
- Phenotypic plasticity underlies local invasion and distant metastasis in colon cancer 96%
- Weakly migratory metastatic breast cancer cells activate fibroblasts via microvesicle-Tg2 to facilitate dissemination and metastasis 96%
- PCK1 and DHODH drive colorectal cancer liver metastatic colonization and nucleotide biosynthesis under hypoxia 96%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.