Curcumin suppresses cell proliferation and triggers apoptosis in vemurafenib‐resistant melanoma cells by downregulating the EGFR signaling pathway

• Published in: Environmental toxicology Vol. 37; no. 4; pp. 868 - 879
• Main Authors: Chiu, Yu‐Jen, Yang, Jai‐Sing, Tsai, Fuu‐Jen, Chiu, Hong‐Yi, Juan, Yu‐Ning, Lo, Yu‐Hsiang, Chiang, Jo‐Hua
• Format: Journal Article
• Language: English
• Published: Hoboken, USA John Wiley & Sons, Inc 01.04.2022; Wiley Subscription Services, Inc
• Subjects: aggression; Aggressive behaviour; AKT protein; Apoptosis; Caspase; Cell Line, Tumor; Cell Proliferation; Cell viability; Cells; Curcumin; Curcumin - pharmacology; Curcumin - therapeutic use; Cytotoxicity; drug resistance; Drug Resistance, Neoplasm; ecotoxicology; EGFR; Epidermal growth factor; Epidermal growth factor receptors; ErbB Receptors - genetics; ErbB Receptors - metabolism; Extracellular; Extracellular signal-regulated kinase; Gefitinib; Growth factors; Humans; Inhibitor drugs; Inhibitors; Kinases; Melanoma; Melanoma - drug therapy; Melanoma - genetics; Melanoma - pathology; Membrane potential; Mitochondria; mitochondrial membrane; mitogen-activated protein kinase; Mutation; Neoplasms; Proliferation; Protein-serine/threonine kinase; Reactive oxygen species; Serine; Signal Transduction; Signaling; therapeutics; Threonine; Tumors; vemurafenib; Vemurafenib - pharmacology; Vemurafenib - therapeutic use; vemurafenib‐resistant A375.S2 cells; vemurafenib; apoptosis; melanoma; EGFR; vemurafenib-resistant A375.S2 cells

Melanoma is a malignant tumor with aggressive behavior. Vemurafenib, a BRAF inhibitor, is clinically used in melanoma, but resistance to melanoma cytotoxic therapies is associated with BRAF mutations. Curcumin can effectively inhibit numerous types of cancers. However, there are no reports regarding...