fig4

The role of melatonin as an adjuvant therapeutic strategy in the modulation of carcinogenesis. A narrative review

Figure 4. Anticancer action mechanisms of melatonin. →: Promote; −ǀ: inhibit; −: modulate; NF-κβ: nuclear factor kappa B; TGF-β: transforming growth factor beta; PGE2: prostaglandin E2; EGFR: Epidermal growth factor receptor; PI3K: phosphoinositol 3-kinases; mTOR: mammalian Target of Rapamycin; MAPK/ERK: mitogen-activated protein kinases; JNK: c-Jun N-terminal kinase; IGF-1: insulin grow factor 1; CDKs: cyclin-dependent kinases; hTERT: human telomerase reverse transcriptase; SEEM: selective estrogen enzyme modulator; SERM: selective estrogen receptor modulator; ER: estrogen receptor; CaM: Calmodulin; AIF: apoptosis-inducing factor; XIAP: X-linked inhibitor of apoptosis; PAIs: inhibit the apoptosis process; MMP: metalloproteinases; EMT: epithelial-mesenchymal transition; VEGF: vascular endothelial growth factor; VEGFR2: vascular endothelial growth factor receptor 2; HIF: hypoxia-inducing factor; STAT3: signal transducer and activator of transcription 3; ET1: Endothelin-1; PDKs: phosphoinositide-dependent protein kinase; LA: lactic acid; 13-HODE: 13-hydroxyoctadecadienoic acid; Nrf2: nuclear factor erythroid 2; SIRT3: sirtuin 3; miRNA: microRNAs; SOD2: superoxide dismutase; GPX3: glutathione peroxidase.

Journal of Cancer Metastasis and Treatment
ISSN 2454-2857 (Online) 2394-4722 (Print)

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All published articles are preserved here permanently:

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