Application of nanotechnology in reversing therapeutic resistance and controlling metastasis of colorectal cancer

Figure 1 Schematic illustration of mechanisms of colorectal cancer cell resistance to chemotherapy, radiotherapy, immunotherapy, targeted therapy, and metastasis. ABC: ATP binding cassette; B2M: β2-microglobulin; CAFs: Cancer associated fibroblasts; CIMP: CpG island methylator phenotype; CIN: Chromosomal instability; CTC: Circulating tumor cell; CYP3A4: Cytochrome P450 3A4; DPD: Dihydropyrimidine dehydrogenase; EGFR: Epidermal growth factor receptor; EMT: Epithelial-mesenchymal transition; ERBB2: Erb-b2 receptor tyrosine kinase 2; ERK2: Extracellular regulated protein kinases; HGF: Hepatocyte growth factor; hMLH1: Human MutL homolog 1; HSP27: Heat shock protein 27; IGF-1R: Insulin-like growth factor 1 receptor; ILC3s: Group 3 innate lymphoid cells; MAPKAPK2: Mitogen-activated protein; MDSCs: Myeloid-derived suppressive cells; MSI: Microsatellite instability; NETs: Neutrophil extracellular traps; NF1: Neurofibromin 1; p38MAPK: p38 mitogen-activated protein kinase; PP2A: Protein phosphatase 2A; SLC: Solute carrier; TAP1: Transporter 1; TAP2: Transporter 2; TAMs: Tumor associated macrophages; TME: Tumor microenvironment; TOP-1: Topoisomerase 1; TP: Thymine phosphorylase; TRAP1: TNF receptor associated protein 1; TS: Thymidylate synthase; UGT1A: Uridine diphosphate glucuronosyltransferase 1A.