Nicotinamide Mononucleotide Adenylyl Transferase 2: A Promising Diagnostic and Therapeutic Target for Colorectal Cancer.

Nicotinamide Mononucleotide Adenylyl Transferase 2: A Promising Diagnostic and Therapeutic Target for Colorectal Cancer.
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DOI:
10.1155/2016/1804137
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发表时间:
2016
影响因子:
--
通讯作者:
Yu J
Yu J
中科院分区:
生物学3区
文献类型:
--
作者:
Cui C;Qi J;Deng Q;Chen R;Zhai D;Yu J

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结直肠癌是世界上最常见的癌症之一。因此,寻找更有效的诊断和治疗方法是至关重要的。烟酰胺腺嘌呤二核苷酸(NAD)代谢异常被认为是癌细胞的特征。在这项研究中,烟酰胺单核苷酸腺苷酸转移酶(NMNATs)以及p53介导的癌症信号通路在结直肠癌患者进行了研究。从95名未经治疗的结直肠癌患者获得CRC组织和邻近的正常组织,并对烟酰胺单核苷酸腺苷酰转移酶2(NMNAT 2)和p53的表达进行染色。生存率采用Kaplan-Meier法和log-rank检验进行分析。同时进行多因素考克斯比例风险回归分析。NMNAT 2和p53在结直肠癌组织中的表达显著增高,且NMNAT 2的表达与肿瘤浸润深度和TNM分期有关。NMNAT 2与p53的表达呈显著正相关。然而,NMNAT 2表达不是总生存率的统计学显著预后因素。结论:NMNAT 2可能以p53依赖的方式参与结直肠癌的发生,NMNAT 2的表达可能是一个潜在的治疗靶点。
Colorectal cancer (CRC) is one of the most common cancers all over the world. It is essential to search for more effective diagnostic and therapeutic methods for CRC. Abnormal nicotinamide adenine dinucleotide (NAD) metabolism has been considered as a characteristic of cancer cells. In this study, nicotinamide mononucleotide adenylyl transferases (NMNATs) as well as p53-mediated cancer signaling pathways were investigated in patients with colorectal cancer. The CRC tissues and adjacent normal tissues were obtained from 95 untreated colorectal cancer patients and were stained for expression of nicotinamide mononucleotide adenylyl transferase 2 (NMNAT2) and p53. The survival rate was analyzed by the Kaplan-Meier method and the log-rank test. The multivariate Cox proportional hazard regression analysis was conducted as well. Our data demonstrated that expression of NMNAT2 and p53 was significantly higher in CRC tissues, while NMNAT2 expression is in correlation with the invasive depth of tumors and TNM stage. Significant positive correlation was found between the expression of NMNAT2 and the expression of p53. However, NMNAT2 expression was not a statistically significant prognostic factor for overall survival. In conclusion, our results indicated that NMNAT2 might participate in tumorigenesis of CRC in a p53-dependent manner and NMNAT2 expression might be a potential therapeutic target for CRC.