Comprehensive transcriptomic analyses describe the underlying tumorigenic gene expression state in the invasive Drosophila follicle cells following the loss of epithelial cell polarity and identify a non-canonical role of Keap1-Nrf2 signaling in regulating collective cell invasion.

Genetic analysis identifies an enzyme of the malaria parasite that is required to seal its host red blood cell membrane upon invasion, a key requirement of this important intracellular pathogen.

siRNA knockdown experiments reveal in detail the signaling pathway that controls cytoskeletal function during cell-in-cell invasion.

Specific localization of KRAS downstream target ARL4C with its novel interacting proteins was the active site of invasion of pancreatic cancer cell and induced metastasis.

Cancer invasion occurs with different molecular and spatial patterns, thin invading strands are associated with mesenchymal cell features, such as low cell-cell adhesion, while broad strands are favoured for lymph node metastasis and require high matrix proteolysis and cell-cell adhesions.

Chromatin-based cancer stem cell heterogeneity typifies primary glioblastoma and includes an invasive subtype associated with a lower survival.

Colon cancer cells disseminate and colonize distant organ sites along the invasion-metastasis cascade by transiently activating intermediate epithelial to mesenchymal transition states through distinct transcriptional trajectories.

A chemical probe was characterized for potency, selectivity, and ability to alter CARM1-dependent epigenetic plasticity against cancer cell invasion.

New role of P2Y₂-αV integrin interactions in ATP-driven pancreatic cancer cell invasion provides a potential anti-metastatic target for pancreatic cancer.

The rhoptry protein RhopH3 is crucial for the invasion and growth of the malaria parasite and disruption of it provides insight into the binding of the parasite to the host red blood cell and into the formation of new import pathways.