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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。
By transducing extracellular signals into the nucleus, mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-hydroxy kinase / protein kinase B (PI3K / Akt) signaling pathways in cell growth, proliferation and apoptosis Activities play an important regulatory role. Multiple abnormal expression of genes encoding MAPK / ERK and PI3K / Akt signaling in thyroid cancer cells. Mutation and interaction of MAPK / ERK and PI3K / Akt signaling pathway caused by gene mutation are closely related to the occurrence and progression of thyroid cancer. This article mainly reviews the gene mutation of MAPK and PI3K / Akt signaling pathway in the occurrence, progression and diagnosis of thyroid carcinoma. In addition, this article will also explore the simultaneous inhibition of MAPK and PI3K / Akt signaling pathway, to restore cell iodine uptake capacity, and to guide the therapeutic potential of radionuclide targeted therapies for thyroid cancer.