pVHL/HIF通路与PI3K/PKB/FOXO通路在肾透明细胞癌发生、发展中的作用

The roles of pVHL/HIF pathway and PI3K/PKB/FOXO pathway in the tumorigenesis and development of the clear cell renal carcinoma(CCRCC)

肿瘤抑制基因vonHipple-Lindau(简称VHL基因)的突变失活导致肿瘤细胞中缺氧诱导因子的累积,进而调节其下游靶基因的转录和表达,促进肿瘤内新生血管形成及细胞增殖,从而促进肾透明细胞癌的发生、发展。磷酸肌醇-3激酶/蛋白激酶B通路异常活化,在肾细胞肿瘤的发生、发展、转移中发挥重要作用。上述两通路存在着错综复杂的联系。本文通过分析两通路在肾肿瘤发生,发展中的作用,为探寻肾癌治疗的新靶点提供理论依据。

The mutation of yon Hippie -Lindau tumor suppressor gene results in the inactivation of pVHL, and abnormal accumulation of hypoxia inducible factor - α（ HIF - α） , HIF - αregulates the transcription and expression of downstream genes, and promotes tumorigenesis and development of the clear cell renal cell carcinoma （ CCRCC ） through stimulating angiogenesis and cell proliferation. The abnormal activation of phosphatidyinositol 3 - kinase/protein kinase B （PI3K/PKB） pathway also plays important roles in tumorigenesis , development and metastasis of the renal cell carcinoma. There are complicated relationships between the two pathways above . This review tries to elucidate the roles of the two pathways in tumorigenesis and development of renal neoplasia , and find out new target of renal tumor therapy in the future for the clinic.