• 1.蘇州大學第一附屬醫(yī)院普外科（蘇州215006）;;
  • 2.廣東醫(yī)學院附屬湛江中心人民醫(yī)院肝膽外科（廣東湛江524037）;;
  • 3.青島大學醫(yī)學院附屬醫(yī)院肝膽外科（山東青島266404）;

目的 　觀察高轉移性人肝癌細胞系HCC9204轉染抑制性κB基因（IκB-α)后核因子-κB(NF-κB)和基質金屬蛋白酶-9（MMP-9)表達的改變。
方法 　采用脂質體法將IκB-α基因轉染HCC9204細胞，應用Western-blot及RT-PCR法檢測MMP-9和NF-κB的表達； 通過基底膜侵襲實驗檢測腫瘤細胞的浸潤和轉移能力。
結果 　HCC9204細胞轉染pcDNA3-IκB-α后，細胞內NF-κB蛋白表達下降，同時伴隨MMP-9 mRNA表達水平和細胞侵襲、轉移能力的明顯下降。
結論 　NF-κB活性被抑制后引起細胞侵襲、轉移能力的下降可能是由于MMP-9表達下降所致。

引用本文： 張克君,高焱明,楊金鏞,張炳遠. IκB-α基因轉染HCC9204細胞對NF-κB和MMP-9表達的影響. 中國普外基礎與臨床雜志, 2007, 14(2): 185-187. doi: 復制

版權信息： ?四川大學華西醫(yī)院華西期刊社《中國普外基礎與臨床雜志》版權所有，未經授權不得轉載、改編

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  2. 2. 　Shukla S, MacLennan GT, Fu P, et al. Nuclear factor-kappa B/p65 (Rel A) is constitutively activated in human prostate adenocarcinoma and correlates with disease progression [Ｊ]. Neoplasia， 2004; 6(4)∶390.
  3. 3. 　Andela VB, Schwarz EM, Puzas JE, et al. Tumor metastasis and the reciprocal regulation of prometastatic and antimetastatic factors by nuclear factor kappa B [Ｊ]. Cancer Res， 2000; 60(23)∶6557.
  4. 4. 　Jiang Y, Cui L, Yie TA, et al. Inhibition of anchorage-independent growth and lung metastasis of A549 lung carcinoma cells by I kappa B beta [Ｊ]. Oncogene， 2001; 20(18)∶2254.
  5. 5. 　Hah N, Lee ST. An absolute role of the PKC-dependent NF-kappa B activation for induction of MMP-9 in hepatocellular carcinoma cells [Ｊ]. Biochem Biophys Res Commun， 2003; 305(2)∶428.
  6. 6. 　Ortega N, Jonca F, Vincent S, et al. Systemic activation of the vascular endothelial growth factor receptor KDR/flk-1 selectively triggers endothelial cells with an angiogenic phenotype [Ｊ]. Am J Pathol, 1997; 151(5)∶1215.
  7. 7. 　Li Z, Ren Y, Wu QC, et al. Macrophage migration inhibitory factor enhances neoplastic cell invasion by inducing the expression of matrix metalloproteinase 9 and interleukin-8 in nasopharyngeal carcinoma cell lines [Ｊ]. Chin Med J (Engl), 2004; 117(1)∶107.
  8. 8. 　張克君， 高焱明， 楊堂斗， 等. 核因子-κB p65、IκB-α在肝炎相關性肝細胞癌中的表達及臨床意義 [Ｊ]. 實用腫瘤雜志， 2004; 19(3)∶216.
  9. 9. 　張克君， 高焱明. 核因子-κB p65在肝炎相關性肝細胞癌中的表達及意義 [Ｊ]. 中國癌癥雜志， 2005； 15（1）∶12.