PI3K/AKT通路在口腔鳞癌中的研究进展

Research Progress of PI3K/AKT Pathway in Oral Squamous Cell Carcinoma

口腔鳞状细胞癌(oral squamous cell carcinoma,OSCC)作为常见的头颈部恶性肿瘤,死亡率较高。磷脂酰肌醇3-激酶/蛋白激酶B(PI3K/AKT)信号通路作为分子传导机制直接参与了多种恶性肿瘤(包括OSCC)的发生发展过程。降低磷酸化PI3K和AKT的表达可以抑制OSCC细胞的进展。因此,本文对PI3K/AKT通路的组成及其对OSCC细胞周期、凋亡、自噬、侵袭与转移,糖酵解以及血管生成等的调节作用,特别是该通路作为靶向抑制剂在OSCC中的使用与发展做一总结。

As a common head and neck malignant tumor,oral squamous cell carcinoma(OSCC)has a high mortality rate.Phosphatidyl inositol 3 kinase/protein kinase B(PI3K/AKT)signal pathway as a molecular conduction mechanism directly involved in a variety of malignant tumors(including OSCC)development process.Decreased expression of phosphorylated PI3K and AKT could inhibit OSCC cell progression.Therefore,this article reviews the composition of PI3K/AKT pathway and its regulatory effects on OSCC cell cycle,apoptosis,autophagy,invasion and metastasis,glycolysis and angiogenesis,especially the use and development of PI3K/AKT pathway as a targeted inhibitor in OSCC,aiming to provide a new target for the diagnosis and treatment of OSCC.