Dual Role of RAD51 in Hepatocellular Carcinoma

• Main Authors: Chia-Jung Tsai, 蔡佳蓉
• Other Authors: Shen-Nien Wang
• Format: Others
• Language: zh-TW
• Published: 2009
• Online Access: http://ndltd.ncl.edu.tw/handle/91181911789780294526

碩士 === 高雄醫學大學 === 醫學研究所 === 97 === RAD51 is the central protein of homologous recombination which repairs DNA double strand breaks. Controversially, RAD51 is also essential for cell proliferation. It is presumably possible that aberrations of RAD51 may play roles in human cancers. However, absent information concerns about its role in hepatocellular carcinoma (HCC). Thus, we aim to disclose such a protein exerting pleiotropic effects through its clinical impacts. Nuclear RAD51 staining in HCC lesions was predominantly decreased and was correlated with recurrence rate in HCC patients (p=0.015). Nuclear RAD51 staining was predominantly decreased and was correlated with Ki-67 index as well as nuclear TP53 frequency in HCC lesions (p=0.002 and 0.004, respectively). Besides, the patients presented with high TP53 intensity, presentence of vascular invasion and positive rate of recurrence had a significantly poor overall survival in the subgroup with a decreased nuclear RAD51 staining (p=0.011, 0.040 and 0.009). Interestingly, overexpression of RAD51 protein increased the proliferation rate of Hep-3B but decreased those of Mahlavu and Hep-G2 cells. We also found that RAD51 increased the migration rate of Mahlavu and Hep-G2 cells but decreased that of Hep-3B cells. Moreover, overexpression of RAD51 decreased p-cofilin levels in Hep-3B cells but increased p-cofilin levels in Mahlavu and Hep-G2 cells. Our results showed that RAD51 may play different roles partly depending on TP53 status in contributing to HCC. In addition, cytoplasmic RAD51 may cooperate with adhesion and actin-remodeling signaling to modulate invasive potential in HCC.