傳遞抑制腫瘤基因p53有潛力發展成治療肝癌腫瘤的方法之一。第二型重組類腺病毒 ( rAAV2 ) 已應用於臨床試驗，相對於其他常用的病毒載體如腺病毒和反轉錄病毒，rAAV2有較高的安全性。然而治療肝癌腫瘤，提升rAAV2對肝癌細胞的轉導效率是必要的。本研究中，我們利用化療藥物Doxorubicin誘導rAAV2轉導肝癌細胞。實驗數據指出：將Doxorubicin和帶有報導基因的rAAV2合併使用，分別對肝癌細胞HepG2 ( p53原生型 ) 與Hep3B ( 缺乏p53 ) 進行轉導，其報導基因表現量比單獨rAAV2轉導的效率分別高出350和120倍；由於效率大幅提升，我們應用攜帶p53基因的rAAV2 ( rAAV2-p53 ) 對肝癌細胞Hep3B進行轉導，使肝癌細胞Hep3B恢復p53的表現。實驗中，將Doxorubicin和rAAV2-p53合併使用對肝癌細胞Hep3B進行轉導，肝癌細胞Hep3B的p53表現量比單獨rAAV2-p53轉導效率高出16倍，而且相較於HepG2原生型p53的表現量更高出380 %。將Doxorubicin ( 0.5 μM ) 和rAAV2-p53 ( MOI = 10 ) 合併作用在肝癌細胞Hep3B ( 12小時 ) ，我們發現96小時後肝癌細胞的生存率下降至66 %，此結果與肝癌細胞Hep3B只有Doxorubicin ( 1 μM ) 單獨作用的生存率相同。上述將Doxorubicin的劑量從1 μM 降到0.5 μM的實驗結果顯示出rAAV2-p53的基因轉導具有抗癌的效果；與其合併Doxorubicin作用時更具有抑制肝癌腫瘤生長的效用。結論，在Doxorubicin作用下，rAAV2-p53對肝癌細胞的轉導效率有明顯提升，因此合併Doxorubicin和rAAV2-p53對治療因p53突變所引起的肝癌 ( Hepatocellular carcinoma, HCC ) 具有加乘的療效。

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