Gefitinib inhibits malignant melanoma cells through the VEGF/AKT signaling pathway
- Xuefeng Wan
- Yalin Zhu
- Lijuan Zhang
- Wei Hou
Published online on: March 13, 2018
Malignant melanoma (MM) is caused by melanophore cancerization in tissue pigmentation regions, leading to skin, mucous membrane, eye and central nervous system carcinogenesis. The incidence of MM has increased in previous years, and it has become the primary cause of skin cancer‑associated mortality in developed countries. MM is characterized as highly malignant and readily metastasized, and has a poor prognosis. Targeting angiogenesis is an important method for MM treatment. As an important proangiogenic factor in tumor growth and metastasis, vascular endothelial growth factor (VEGF) can promote neovascularization and increase vascular permeability. Gefitinib is a novel drug targeting VEGF. The effect and mechanism of gefitinib on MM remain to be elucidated, and were investigated in the present study. The A375 MM cell line was used in the present study; it was cultured in vitro and divided into gefitinib groups (5 and 10 µM) and a control group. Cell proliferation was measured using an MTT assay and the activity of caspase‑3 was assessed using a kit. Cell invasive ability was determined using a Transwell chamber. The mRNA and protein expression levels of VEGF and AKT were detected using reverse transcription‑quantitative polymerase chain reaction and western blot analyses. Gefitinib significantly inhibited MM cell proliferation, enhanced the activity of caspase 3 and suppressed tumor cell invasion (P<0.05). In addition, gefitinib significantly downregulated the mRNA and protein expression levels of VEGF and AKT, and these changes were dose‑dependent (P<0.05). Taken together, gefitinib suppressed MM cell proliferation and invasion in vitro by regulating the VEGF/AKT signaling pathway.