Metastasis
- EML4–ALK V3 oncogenic fusion proteins promote microtubule stabilization and accelerated migration through NEK9 and NEK7
Summary: EML4–ALK fusions are major drivers of lung cancer. Particular fusion variants act through a novel actionable pathway involving NEK7 and NEK9, promoting cell migration and potentially influencing metastatic progression.
- VLA-4 phosphorylation during tumor and immune cell migration relies on its coupling to VEGFR2 and CXCR4 by syndecan-1
Summary: VEGFR2 docked to shed Sdc1 activates CXCR4- and VLA-4-dependent tumor cell migration. Blocking VEGFR2 docking prevents this migration while stimulating the migration of tumor-targeting T cells and NK cells.
- Genetic heterogeneity within collective invasion packs drives leader and follower cell phenotypes
Summary: Image-guided capture and sequencing of invasive cancer cells reveals novel leader- and follower-specific gene mutations, highlighting an important relationship between genomic and phenotypic heterogeneity during collective invasion.
- Circulating tumor cells exit circulation while maintaining multicellularity, augmenting metastatic potential
Highlighted Article: Circulating tumor cell clusters spread throughout the body by using a unique method to exit blood vessels, which grants the tumor cells an increased ability to form secondary tumors.
- Extracellular Hsp90α and clusterin synergistically promote breast cancer epithelial-to-mesenchymal transition and metastasis via LRP1
Summary: Clusterin is identified to interact with extracellular Hsp90α and modulate its pro-metastatic function through increasing the binding affinity of eHsp90α and LRP1.
- The use of decellularised animal tissue to study disseminating cancer cells
Summary: Decellularised matrices derived from discarded animal-house material provide a physiologically relevant 3D-platform for studying cancer cell behaviour that is easy to use, inexpensive and embraces the 3Rs.
- Re-inforcing the cell death army in the fight against breast cancer
Summary: Induction of BIM and BMF function in metastatic breast cancer can aid current treatment strategies.
- LPP3 mediates self-generation of chemotactic LPA gradients by melanoma cells
Highlighted Article: Melanoma cells can create and follow their own gradients of attractant, via a new mechanism by which tumour cells may undergo metastasis.
- The CCR2 3′UTR functions as a competing endogenous RNA to inhibit breast cancer metastasis
Summary: The CCR2 3′UTR acts as a metastasis suppressor by acting as a competing endogenous RNA for STARD13 and thus inhibiting activation of the RhoA–ROCK1–MLC–F-actin pathway in breast cancer cells.