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高转移潜能肝癌细胞株中凋亡相关蛋白的表达及意义 被引量:1

The expression of apoptosis related proteins in hepatocellular carcinoma cell lines with different metastatic potentials Sill
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摘要 目的探讨肝癌细胞转移潜能与凋亡敏感性之间的关系。方法观察不同转移潜能的肝癌细胞株在肿瘤坏死因子-α(TNF-α)及依托泊苷(Etoposide)的作用下的凋亡发生率及Caspase3的活化,Westernblot检测bcl-2及IAP家族蛋白在不同转移潜能肝癌细胞株中的表达。结果TNF-α(10μg/L)作用后48h,高转移潜能肝癌细胞株HCCLM3及转移能力最弱的肝癌细胞株SMMC-7721的凋亡率分别为(91.3±6.5)%及(58.8±2.3)%,MHCC97L细胞的凋亡率则位于两者之间(P≤0.01)。Etoposide(250μmol/L)作用后48h,HCCLM3、MHCC97L及SMMC-772的凋亡发生率分别为(27.0±4.0)%、(34.6±3.8)%及(84.5±1.1)%(P≤0.01)。3种细胞株中Caspase-3的活性也有明显差异。bel-2及IAP家族蛋白表达研究中发现XIAP的表达与肝癌细胞的转移潜能成梯度相关。结论高转移潜能肝癌细胞株耐受多种凋亡刺激,可能与XIAP的过度表达相关。 Objective To discuss the relationship between the apoptotic sensitivity and metastatic potentials of hepatocellular carcinoma. Methods The nuclear staining and Caspase activity were measured for apoptosis in hepatocellular carcinoma cell lines with different metastatic potentials after TNF-α and Etoposide treatments, and the expression of bcl-2 family proteins and IAPs was detected by Western blot. Resuits After treatment with TNF-α (10 μg/L) for 48 h, the apoptosis rate was (91.3 ± 6. 5)% in SMMC-7721 cell with low metastatic potential and (58.8 ±_2.3)% in HCCLM3.cell with high metastatic potential, respectively. The apoptosis rate in HCCLM3, MHCC9"/L and SMMC-'/'/2 after Etoposide (250 μmol/L) treatment for 48 h was (27.0 ± 4. 0) %, (34.6 ±_ 3.8) % and ( 84.5 ± 1.1 ) %, respectively (P≤0.01). The same difference was shown in Caspase 3 activation in there three cell lines. The expression of XIAP was compatible with the metastatic potential in the cell lines after screening the bcl-2 and IAP family proteins. Conclusion The hepatocellular carcinoma with high metastatic potential is more resistant to apoptosis, which may be correlated with the XIAP expression.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2008年第3期316-318,共3页 Chinese Journal of Experimental Surgery
基金 上海市卫生局科研课题(2006017)
关键词 肝细胞 转移 脱噬作用 Carcinoma,hepatocellular Metastasis Apoptosis
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参考文献3

  • 1Cory S, Adams JM. The bcl-2 family: regulators of the cellular life-or- death switch. Nat Rev Cancer,2002,2:647-656.
  • 2Chiu CT,Yeh TS,Hsu JC,et al. Expression of bcl-2 family modulated through p53-dependent pathway in human hepatocellular carcinoma. Dig Dis Sci ,2003,48:670-676.
  • 3Nachmias B, Ashhab Y, Ben-Yehuda D. The inhibitor of apoptosis protein family ( IAPs ) : an emerging therapeutic target in cancer. Semin Cancer Biol,2004,14:231-243.

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  • 1彭创,汤恢焕,吴金术.Bcl-2反义寡核苷酸对VP-16抑制人胆管癌细胞株增殖和诱导凋亡的影响[J].中国普通外科杂志,2007,16(2):125-128. 被引量:3
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