Fig. 1

Epithelial-mesenchymal transition (EMT), metastasis, cancer stem cells (CSCs), and oncogenic metabolism. Cancer cells can acquire multiple capabilities, including sustained proliferation, evasion of growth suppression, cell death resistance, replicative immortality, evasion of immune destruction, tumour-promoting inflammation, activation of invasion and metastasis, induction of angiogenesis, genome instability, and alteration of metabolism. Deregulation of differentiation, acquisition of stem cell phenotypes, and their tumour microenvironment are also important aspects of tumourigenesis. Several signal pathways (such as those of TGF-β, Wnt, EGF, Hedgehog, Notch, and ROS) and mutation/genomic instability are closely associated with tumourigenesis and tumour progression. These signals could activate oncogenes and inactivate tumour suppressors. Activation of oncogenes, or loss of tumour suppressors, can drive tumour progression, particularly via metabolic reprogramming. Metabolic reprogramming may be required for malignant transformation and tumour development, including invasion and metastasis, CSC phenotype, and TME