Inactivation of a multifunctional RNA-binding protein can lead to the acquisition of pro-metastatic phenotypes, possibly by stabilizing large-scale transcriptomic changes that provide a selective advantage during cancer progression.
Mucins, long associated with cancer aggression, remodel the cancer glycocalyx in a way that promotes proliferation in the metastatic site by enhancing integrin-mediated adhesion and thus driving cell cycle progression.
MYC and Twist1 drive metastasis by a novel non-cell-autonomous transcriptional mechanism of eliciting a cytokinome that mediates the crosstalk between cancer cells and macrophages, and its therapeutic blockade inhibits metastasis.
Syngeneic tp53-null zebrafish develop a wide range of tumors that engraft into recipient animals with loss of Tp53 leading to increased metastasis in embryonal rhabdomyosarcoma (ERMS), likely accounting for increased aggression in TP53-inactivated human ERMS.
Development and application of highly sensitive in situ transcriptomics method, Flura-seq, in identifying dynamic organ-specific transcriptomes in early stage breast cancer metastasis have been described.
In small cell lung cancer, the transition from a neuroendocrine state to a more neuronal state endows these cancer cells with increased migration and metastatic potential.
Many extracellular matrix proteins that are up-regulated during breast tumor progression enhance metastasis, and some are prognostic indicators of poor survival.
The melanoma cell interaction with lymphatic endothelial cells promotes melanoma metastasis by inducing a reversible switch to invasively sprouting melanoma cells.
