The sleeping ugly: Tumour microenvironment's act to make or break the spell of dormancy.

Metastasis is the main cause of death for most cancer patients. It appears clear from clinical observations that the majority of cancers, particularly carcinoma do not follow a linear model of metastatic progression, where cancer cells shed from the primary tumour, disseminate to a distant organ and immediately outgrow to form clinical metastasis. Certainly, while cancer spreading is an early event, metastasis occurs much later during tumour progression and frequently arises several years after primary tumour resection.

Host endothelial S1PR1 regulation of vascular permeability modulates tumor growth.

Understanding vascular growth and maturation in developing tumors has important implications for tumor progression, spread, and ultimately host survival. Modulating the signaling of endothelial G protein-coupled receptors (GPCRs) in blood and lymphatic vessels can enhance or limit tumor progression. Sphingosine 1-phosphate receptor 1 (S1PR1) is a GPCR for circulating lysophospholipid S1P that is highly expressed in blood and lymphatic vessels.

Mitochondrial complex I activity and NAD+/NADH balance regulate breast cancer progression.

Despite advances in clinical therapy, metastasis remains the leading cause of death in breast cancer patients. Mutations in mitochondrial DNA, including those affecting complex I and oxidative phosphorylation, are found in breast tumors and could facilitate metastasis. This study identifies mitochondrial complex I as critical for defining an aggressive phenotype in breast cancer cells.

Platelets alter tumor cell attributes to propel metastasis: programming in transit.

Metastasis of epithelial tumors critically depends on acquisition of a disseminating phenotype that allows tumor cells to colonize distant organs. In this issue of Cancer Cell, Labelle et al. demonstrate that an epithelial-mesenchymal-like transition can be induced by interaction between platelets and tumor cells.

Contribution of platelets to tumour metastasis.

Extensive experimental evidence shows that platelets support tumour metastasis. The activation of platelets and the coagulation system have a crucial role in the progression of cancer. Within the circulatory system, platelets guard tumour cells from immune elimination and promote their arrest at the endothelium, supporting the establishment of secondary lesions.

Spatial mapping of the neurite and soma proteomes reveals a functional Cdc42/Rac regulatory network.

Neurite extension and growth cone navigation are guided by extracellular cues that control cytoskeletal rearrangements. However, understanding the complex signaling mechanisms that mediate neuritogenesis has been limited by the inability to biochemically separate the neurite and soma for spatial proteomic and bioinformatic analyses. Here, we apply global proteome profiling in combination with a neurite purification methodology for comparative analysis of the soma and neurite proteomes of neuroblastoma cells.