Keywordscell fate decision; cancer attractors; gene network dynamics; EMT; therapy resistance; intrinsically disordered proteins; chromatin modifications; EMT; Epigenetics; Epitranscriptomics; EZH2; non-coding RNAs; NSCLC; SCLC; epithelial-mesenchymal transition; tumor progression; metastasis; TGF-β; non-coding RNA; tRNA; post-transcriptional regulation; epithelial-to-mesenchymal transition; mesenchymal-to-epithelial transition; head and neck cancer; biomarkers; EMT; EPT; SRF; myocardin-related transcription factors (MRTF); pericyte; resistance; vascular niche; angiocrine factors; spheroids; EMT/MET; TGF-β; EGR-1; epithelial-mesenchymal transition; microRNAs; lung neoplasms; biomarkers; tumour; ovarian cancer; intraperitoneal metastasis; cadherins; heterogeneity; epithelial-to-mesenchymal transition (EMT); mesenchymal-to-epithelial transition (MET); intraperitoneal tumor microenvironment; computational modeling of EMT; epithelial-mesenchymal transition; exosomes; neoplasm metastasis; neovascularization; pathologic; neoplasm invasiveness; intercellular signaling peptides and proteins; protein kinase CK2; stem cell; breast cancer; EMT; epithelial plasticity; pancreatic cancer; EMT; resistance; PLK1; EMT; tumor invasion and metastasis; drug resistance; cancer therapy; breast cancer; TNBC; EMT; tumor plasticity; molecular signaling; exosomes; miRNAs; αvβ3; differentiation therapy; EMT; colorectal cancer; metastasis; n/a; n/a
