基于PI3K/AKT信号通路探讨中医药治疗甲状腺癌的作用机制  

Action Mechanism of Traditional Chinese Medicine in Treatment of Thyroid Cancer Based on PI3K/AKT Signaling Pathway

在线阅读下载全文

作  者:向中山 王立祚 张格松 张浩利 向建军 XIANG Zhongshan;WANG Lizuo;ZHANG Gesong;ZHANG Haoli;XIANG Jianjun(Hubei University for Nationalities,Enshi Hubei China 445000;Enshi Tujia and Miao Autonomous Prefecture Central Hospital,Enshi Hubei China 445000;Henan University of Chinese Medicine,Zhengzhou Henan China 450046)

机构地区:[1]湖北民族大学,湖北恩施445000 [2]恩施土家族苗族自治州中心医院,湖北恩施445000 [3]河南中医药大学,河南郑州450046

出  处:《中医学报》2025年第4期688-694,共7页Acta Chinese Medicine

基  金:湖北省中医药管理局面上项目(ZY2023M059)。

摘  要:甲状腺癌是全球常见的内分泌恶性肿瘤,其发病率及病死率逐年增高,且具有很强的隐匿性,在早期不易被识别。磷脂酰肌醇3-激酶(phosphatidylinositol 3-kinase,PI3K)/蛋白激酶B(protein kinase B,AKT)信号通路可以调控机体内细胞功能,包括细胞的生长、增殖、凋亡、侵袭,并参与肿瘤细胞恶性增殖、转移等过程。中医药通过调控PI3K/AKT信号通路,可促使肿瘤细胞周期停滞,从而抑制肿瘤细胞增殖、分化;通过抑制上皮间质转化,从而阻止甲状腺癌细胞侵袭、转移;上调自噬相关蛋白的表达,促进甲状腺癌细胞自噬;纠正甲状腺癌糖代谢紊乱,抑制甲状腺癌的发生发展。Thyroid cancer is a common endocrine malignant tumor in the world,and its morbidity and mortality are increasing year by year,and it is very insidious and not easy to be recognized in the early stage.Phosphatidylinositol 3-kinase(PI3K)/protein kinase B(AKT)signaling pathway can regulate cellular functions in the body,including cell growth,proliferation,apoptosis,invasion,and participate in the process of malignant proliferation and metastasis of tumor cells.By regulating the PI3K/AKT signaling pathway,traditional Chinese medicine(TCM)can induce tumor cell cycle arrest,thus inhibiting tumor cell proliferation and differentiation;inhibit epithelial mesenchymal transition,thus preventing thyroid cancer cells from invasion and metastasis;up-regulate the expression of autophagy-related proteins,thus promoting the autophagy of thyroid cancer cells and correct the disorders of glucose metabolism of thyroid cancer,thus inhibiting the occurrence and development of thyroid cancer.

关 键 词:PI3K/AKT信号通路 甲状腺癌 细胞增殖 细胞凋亡 细胞自噬 细胞侵袭 

分 类 号:R273[医药卫生—中西医结合]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象