Wu Meng, Zhang Zhihua, Ma Fangxu, Zhang Xiulong, Zhang Zhilin, Tang Jianhua, Chen Ping, Zhou Chunyan, Wang Weiping
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education of China, Peking University, Beijing 100191, P.R. China.
Department of Respiration, First Affiliated Hospital of Hebei North University, Zhangjiakou, Heibei 075061, P.R. China.
Oncol Lett. 2018 Apr;15(4):5175-5180. doi: 10.3892/ol.2018.7912. Epub 2018 Jan 31.
TAp73 and p53 are involved in regulating tumor angiogenesis and vasohibin-1 (VASH1) is an anti-angiogenic factor. Whether TAp73 regulates angiogenesis positively or negatively is controversial. The status of P53 may determine the effect of TAp73 on angiogenesis. To the best of our knowledge it has not been previously reported whether TAp73, p53 and VASH1 are coexpressed in lung cancer. We profiled the association between TAp73 and p53 and VASH1 expression in lung adenocarcinoma (LAC) and investigated the function of TAp73 in regulating tumor angiogenesis. TAp73, p53 and VASH1 expression in 53 human LAC tissues and the adjacent normal tissues were evaluated using immunohistochemistry. The positive expression rates of p53, TAp73 and VASH1 were significantly higher (92.6, 97.7 and 67.4%, respectively) in LAC tissue compared with paraneoplastic lung tissue (7.4, 2.3 and 32.6%, respectively, P<0.01). Pearson's correlation coefficient showed a significant positive correlation between p53 and TAp73 (r=0.474, P<0.01) and TAp73α and VASH1 (r=0.367, P<0.01). The positive expression rate of p53 and VASH1 was almost significantly correlated (r=0.187, P=0.055). Similarly, p53 expression intensity had a significant positive correlation with TAp73α (r=0.517, P<0.01) and with VASH1 (r=0.277, P<0.01), as did TAp73α with VASH1 (r=0.351, P<0.01). TAp73, p53 (mutant) and VASH1 expression was significantly higher in LAC tissue compared with paraneoplastic lung tissue. The expression trends of the three proteins were significantly positively correlated with each other in LAC. These results suggest that TAp73 may suppress tumor angiogenesis in LAC.
TAp73和p53参与调节肿瘤血管生成，而血管抑制素-1（VASH1）是一种抗血管生成因子。TAp73对血管生成的调节作用是正向还是负向存在争议。p53的状态可能决定TAp73对血管生成的影响。据我们所知，此前尚未报道TAp73、p53和VASH1在肺癌中是否共表达。我们分析了肺腺癌（LAC）中TAp73与p53以及VASH1表达之间的关联，并研究了TAp73在调节肿瘤血管生成中的功能。采用免疫组织化学方法评估了53例人LAC组织及其相邻正常组织中TAp73、p53和VASH1的表达。与癌旁肺组织相比，LAC组织中p53、TAp73和VASH1的阳性表达率显著更高（分别为92.6%、97.7%和67.4%），而癌旁肺组织中的阳性表达率分别为7.4%、2.3%和32.6%（P<0.01）。Pearson相关系数显示p53与TAp73之间存在显著正相关（r=0.474，P<0.01），TAp73α与VASH1之间也存在显著正相关（r=0.367，P<0.01）。p53与VASH1的阳性表达率几乎呈显著相关（r=0.187，P=0.055）。同样，p53的表达强度与TAp73α呈显著正相关（r=0.517，P<0.01），与VASH1也呈显著正相关（r=0.277，P<0.01），TAp73α与VASH1之间也是如此（r=0.351，P<0.01）。与癌旁肺组织相比，LAC组织中TAp73、p53（突变型）和VASH1的表达显著更高。在LAC中，这三种蛋白的表达趋势彼此显著正相关。这些结果表明TAp73可能抑制LAC中的肿瘤血管生成。
