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Weakly migratory cancer cells facilitate their own escape from the primary tumor by releasing microvesicles that activate fibroblasts to remodel matrix and facilitate cancer cell metastasis.

PRMT7-mediated SHANK2 methylation regulates breast cancer metastasis by activating endosomal FAK signals, and may provide potential clues for tumour metastasis treatment strategies.

Specific tissue environments provide selective pressures that give rise to distinct Ras oncogenic dosage in primary liver tumours and their metastatic-like outgrowths.

Genetic mouse models and human cell lines show that Musashi proteins promote an epithelial/luminal state and inhibit epithelial–mesenchymal transition (EMT), and genome-wide maps of translational regulatory targets connect Musashi proteins to an epithelial alternative splicing program and to the regulation of EMT.

Multiplexing and digital analysis of melanoma tissue describe functionally the microenvironment associated with brisk/non-brisk infiltrates and expose the functional incongruences of this morphological classification currently in use for tumor-infiltrating lymphocytes.

The inhibition of colorectal cancer (CRC) proliferation, migration, and invasion is attributed to BEST4, which exhibits epistasis over Hes4 in the downregulation of Twist1 and consequent suppression of epithelial-to-mesenchymal transition in CRC.

A single-cell landscape of acral melanoma and the intermolecular regulatory relationships between microenvironments.

Somatic mutations frequently disrupt cleavage and polyadenylation signals in tumour suppressor genes in human cancers, likely contributing to tumour progression.

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.

A biomechanical approach inducing confined cell migration reveals that mechanical stress has a profound effect on cancer cell survival.