[1]李荣宾,黄延延,林贤宾,等.IGF1/RPI3K/Akt通路及其调控对非小细胞肺癌血管生成拟态形成影响的研究[J].福建医药杂志,2023,45(03):112-115.
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IGF1/RPI3K/Akt通路及其调控对非小细胞肺癌血管生成拟态形成影响的研究()
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《福建医药杂志》[ISSN:1002-2600/CN:35-1071/R]

卷:
45
期数:
2023年03期
页码:
112-115
栏目:
基础研究
出版日期:
2023-06-15

文章信息/Info

文章编号:
1002-2600(2023)03-0112-04
作者:
李荣宾黄延延1林贤宾杨建胜
福建医科大学附属第二医院胸外科(泉州 362000)
关键词:
非小细胞肺癌 抗血管生成 KLF16 IGF1R/PI3K/Akt 血管生成拟态
分类号:
R734.2
文献标志码:
A
摘要:
目的 为非小细胞肺癌(NSCLC)的治疗探索一个潜在的分子靶标。方法 通过qPCR、Western blot、免疫组化检测NSCLC组织和癌旁组织KLF16、IGF1R表达情况; 通过抑制IGF1R/PI3K/Akt通路活化,检测相关靶标MMP2和MMP9的表达; 通过IGF1R/PI3K/Akt通路抑制剂LY294002干预血管生成拟态(VM)形成。结果 与癌旁组织相比,免疫组化、Western blot和qPCR提示,KLF16在NSCLC组织中表达降低,且随着NSCLC级别提高,表达量递减。NSCLC组织中存在明显IGF1R阳性,且IGF1R阳性表达量随着NSCLC级别增高而递增。同时,Western blot和Matrigel三维细胞培养结果表明,随着IGF1R/PI3K/Akt通路抑制剂浓度增加,IGF1R/PI3K/Akt通路相关蛋白质、MMP2、MMP9表达水平也随之降低,肿瘤VM形成随之减少。结论 NSCLC VM的形成与IGF1R/PI3K/Akt信号通路有关,KLF16在NSCLC中的表达趋势与IGF1R表达相反,两者之间是否存在调控关系需进一步验证。

参考文献/References:

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备注/Memo

备注/Memo:
基金项目:福建省自然科学资金资助项目(2019J01477)
1 福建医科大学附属第二医院超声医学科
更新日期/Last Update: 2023-06-15