摘要
通过将细胞外信号转导至细胞核内,丝裂原活化蛋白激酶(MAPK)和磷脂酰肌醇-3羟基激酶/蛋白激酶B(PI3K/Akt)信号通道在细胞的生长、增殖及凋亡等活动中发挥着重要的调节作用。甲状腺癌细胞MAPK/ERK和PI3K/Akt信号通道蛋白的编码基因多异常表达。基因变异致MAPK/ERK和PI3K/Akt信号通道的过度活化及相互作用,与甲状腺癌的发生及进展密切相关。本文主要就MAPK和PI3K/Akt信号通道的基因变异在甲状腺癌发生、进展及诊断中的作用作一综述。此外,本文还将探讨同步抑制MAPK和PI3K/Akt信号通道,恢复细胞的摄碘能力,介导放射性核素靶向治疗甲状腺癌的治疗潜力。
The mitogen-activated protein kinase/extracellular signal-regulated kinase （ MAPK/ERK ） and phoshoinositide-3-kinase/protein kinase B （PI3K/Akt） signaling pathways play a major role in regulating cell growth, proliferation and apoptosis, via transmission of cell signals to cell nucleus. The genes, coding the MAPK/ ERK and PI3K/Akt signaling cascade proteins, are significantly mutated in thyroid cancer. Genetic alternations con- tribute to aberrant activations and interaction of MAPK/ERK and PI3K/Akt signaling pathways in consequence of malignant follicular cell transformation and progression. This review focuses mainly on the role of genetic alterations in coding MAPK/ERK and PI3K/Akt signaling pathway proteins in generation, progression and diagnosis of thyroid cancer. Moreover, it additionally points out a therapeutic potential in restoring iodine avidity of thyroid cancer cells for radionuclide targeted treatment, by synergistically inhibiting activity of signaling pathways.
出处
《生物医学工程学杂志》
EI
CAS
CSCD
北大核心
2012年第6期1221-1225,共5页
Journal of Biomedical Engineering
基金
国家自然科学基金资助项目(81071184)
卫生行业科研专项项目子课题<甲状腺疾病的诊断及治疗>资助(201002002)
