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.
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.
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.
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.
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.
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.
When pioneer metastatic cells enter a sentinel lymph node through afferent lymphatics subcapsular sinus, macrophages provide them soil to proliferate and colonize lymph node.
The gluconeogenic enzyme PCK1 and pyrimidine nucleotide biosynthetic enzyme DHODH drive hypoxic pyrimidine nucleotide biosynthesis and liver metastatic colonization in colorectal cancer, which is therapeutically exploitable by DHODH pharmacologic inhibition.
