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[1]李榮賓,黃延延,林賢賓,等.IGF1/RPI3K/Akt通路及其調(diào)控對非小細(xì)胞肺癌血管生成擬態(tài)形成影響的研究[J].福建醫(yī)藥雜志,2023,45(03):112-115.
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IGF1/RPI3K/Akt通路及其調(diào)控對非小細(xì)胞肺癌血管生成擬態(tài)形成影響的研究()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
45
期數(shù):
2023年03期
頁碼:
112-115
欄目:
基礎(chǔ)研究
出版日期:
2023-06-15

文章信息/Info

文章編號:
1002-2600(2023)03-0112-04
作者:
李榮賓黃延延1林賢賓楊建勝
福建醫(yī)科大學(xué)附屬第二醫(yī)院胸外科(泉州 362000)
關(guān)鍵詞:
非小細(xì)胞肺癌 抗血管生成 KLF16 IGF1R/PI3K/Akt 血管生成擬態(tài)
分類號:
R734.2
文獻(xiàn)標(biāo)志碼:
A
摘要:
目的 為非小細(xì)胞肺癌(NSCLC)的治療探索一個(gè)潛在的分子靶標(biāo)。方法 通過qPCR、Western blot、免疫組化檢測NSCLC組織和癌旁組織KLF16、IGF1R表達(dá)情況; 通過抑制IGF1R/PI3K/Akt通路活化,檢測相關(guān)靶標(biāo)MMP2和MMP9的表達(dá); 通過IGF1R/PI3K/Akt通路抑制劑LY294002干預(yù)血管生成擬態(tài)(VM)形成。結(jié)果 與癌旁組織相比,免疫組化、Western blot和qPCR提示,KLF16在NSCLC組織中表達(dá)降低,且隨著NSCLC級別提高,表達(dá)量遞減。NSCLC組織中存在明顯IGF1R陽性,且IGF1R陽性表達(dá)量隨著NSCLC級別增高而遞增。同時(shí),Western blot和Matrigel三維細(xì)胞培養(yǎng)結(jié)果表明,隨著IGF1R/PI3K/Akt通路抑制劑濃度增加,IGF1R/PI3K/Akt通路相關(guān)蛋白質(zhì)、MMP2、MMP9表達(dá)水平也隨之降低,腫瘤VM形成隨之減少。結(jié)論 NSCLC VM的形成與IGF1R/PI3K/Akt信號通路有關(guān),KLF16在NSCLC中的表達(dá)趨勢與IGF1R表達(dá)相反,兩者之間是否存在調(diào)控關(guān)系需進(jìn)一步驗(yàn)證。

參考文獻(xiàn)/References:

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備注/Memo

備注/Memo:
基金項(xiàng)目:福建省自然科學(xué)資金資助項(xiàng)目(2019J01477)
1 福建醫(yī)科大學(xué)附屬第二醫(yī)院超聲醫(yī)學(xué)科
更新日期/Last Update: 2023-06-15