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.
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.
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.
Many extracellular matrix proteins that are up-regulated during breast tumor progression enhance metastasis, and some are prognostic indicators of poor survival.
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.
A photoconversion-based isolation technique enables systematic investigation of spatially distinct small metastases (microcolonies) versus large lesions (macrometastases).
When pioneer metastatic cells enter a sentinel lymph node through afferent lymphatics subcapsular sinus, macrophages provide them soil to proliferate and colonize lymph node.
Carbonyl stress mediated by Methylglyoxal affects Hsp90 activity, inhibits the Hippo pathway and promotes tumor growth and metastasis in breast cancer.
