Smalley K, Eisen T
Department of Oncology, University College London, 91 Riding House Street, W1P 8BT, London, UK.
FEBS Lett. 2000 Jul 7;476(3):198-202. doi: 10.1016/s0014-5793(00)01726-9.
Activation of p38 or p44/42 mitogen-activated protein (MAP) kinases has been shown to trigger differentiation in a number of cell types. The present study has investigated the roles of these kinases in the alpha-melanocyte stimulating hormone (alpha-MSH)-induced melanogenic and proliferative responses in B16 melanoma cells. Treatment of cells with alpha-MSH led to the time-dependent phosphorylation of both p38 and p44/42 MAP kinases. However, only inhibition of p38 MAP kinase activity with SB 203580 blocked both the alpha-MSH-induced melanogenic and anti-proliferative effects. It therefore appears that activation of the p38 pathway can promote melanogenesis and inhibit growth of B16 melanoma cells.
已表明p38或p44/42丝裂原活化蛋白(MAP)激酶的激活可触发多种细胞类型的分化。本研究调查了这些激酶在α-黑素细胞刺激激素(α-MSH)诱导的B16黑色素瘤细胞的黑素生成和增殖反应中的作用。用α-MSH处理细胞导致p38和p44/42 MAP激酶的时间依赖性磷酸化。然而,只有用SB 203580抑制p38 MAP激酶活性才能阻断α-MSH诱导的黑素生成和抗增殖作用。因此,似乎p38途径的激活可促进B16黑色素瘤细胞的黑素生成并抑制其生长。