烟酰胺腺嘌呤二核苷酸激酶2在恶性脑肿瘤中的普遍标志性表达

高维 董士业 潘飞燕 刘丹慧*

doi:10.16098/j.issn.0529-1356.2015.05.002

解剖学报 ›› 2015, Vol. 46 ›› Issue (5) : 587-590. DOI: 10.16098/j.issn.0529-1356.2015.05.002

神经生物学

烟酰胺腺嘌呤二核苷酸激酶2在恶性脑肿瘤中的普遍标志性表达

高维董士业潘飞燕刘丹慧*

作者信息 +

Nicotinamide adenine dinucleotide kinase 2 is highly expressed in malignant brain tumors

GAO Wei DONG Shi-ye PAN Fei-yan LIU Dan-hui*

Author information +

文章历史 +

摘要

目的检测烟酰胺腺嘌呤二核苷酸激酶2（NADK2）在恶性脑肿瘤中的表达。方法使用免疫组织化学法检测了NADK2在75例恶性脑肿瘤中的表达。结果本实验检测了NADK2在75例恶性脑肿瘤中的表达情况，包括55例星形细胞瘤、13例少突神经细胞瘤、3例髓母细胞瘤和4例室管膜瘤，74例样本中NADK2的表达都明显高于正常对照组织。对免疫组织化学结果进行吸光度分析，比较NADK2在不同肿瘤类型和不同分级的脑肿瘤中的表达，结果表明，NADK2在恶性脑肿瘤中的表达与肿瘤类型和分级无关。结论高表达NADK2是恶性脑肿瘤的一个普遍特征。

Abstract

Objective To investigate the nicotinamide adenine dinucleotide kinase 2 (NADK2) expression level in malignant brain tumors.Methods Immunohistochemistry analysis was used to analyze the NADK2 expression level in 75 malignant brain tumors including 55 of astrocytoma, 13 of oligodendroglioma, 3 of medulloblastoma and 4 of ependymoma. The integrated absorbance (IA) was measured by ImageJ software. Results The immunohistochemistry results showed that 74/75 tumor samples showed strong NADK2 staining. The IA results suggested that there was no significant difference between different brain tumor types as well as grades. Conclusion The results indicate that high expression of NADK2 is a general characteristic of malignant brain tumors.

导出引用

高维董士业潘飞燕刘丹慧*. 烟酰胺腺嘌呤二核苷酸激酶2在恶性脑肿瘤中的普遍标志性表达[J]. 解剖学报. 2015, 46(5): 587-590 https://doi.org/10.16098/j.issn.0529-1356.2015.05.002

GAO Wei DONG Shi-ye PAN Fei-yan LIU Dan-hui*. Nicotinamide adenine dinucleotide kinase 2 is highly expressed in malignant brain tumors[J]. Acta Anatomica Sinica. 2015, 46(5): 587-590 https://doi.org/10.16098/j.issn.0529-1356.2015.05.002

参考文献

［1］Xu P, Sauve AA. Vitamin B3, the nicotinamide adenine dinucleotides and aging［J］. Mech Ageing Dev, 2010, 131(4):287-298.
［2］Heitzer T, Wenzel U, Hink U, et al. Increased NAD(P)H oxidasemediated superoxide production in renovascular hypertension: evidence for an involvement of protein kinase C［J］. Kidney Int, 1999, 55(1):252-260.
［3］Petrelli R, Felczak K, Cappellacci L. NMN/NaMN adenylyltransferase (NMNAT) and NAD kinase (NADK) inhibitors: chemistry and potential therapeutic applications［J］. Curr Med Chem,2011, 18(13):1973-1992.
［4］Zhang R. MNADK, a long-awaited human mitochondrion-localized NAD kinase［J］. J Cell Physiol, 2015,230(8):1697-1701.
［5］Zhang R. MNADK, a novel liver-enriched mitochondrion-localized NAD kinase［J］. Biol Open,2013, 2(4):432-438.
［6］Ohashi K, Kawai S, Murata K. Identification and characterization of a human mitochondrial NAD kinase［J］. Nat Commun, 2012, 3:1248.
［7］Kahn K, Finkel A. It is a tumor——current review of headache and brain tumor［J］. Curr Pain Headache Rep, 2014, 18(6):421.
［8］Woodworth GF, Dunn GP, Nance EA, et al. Emerging insights into barriers to effective brain tumor therapeutics［J］. Front Oncol, 2014, 4:126.
［9］Pollak N, Niere M, Ziegler M. NAD kinase levels control the NADPH concentration in human cells［J］. J Biol Chem, 2007, 282(46):33562-33571.
［10］Lerner F, Niere M, Ludwig A, et al. Structural and functional characterization of human NAD kinase［J］. Biochem Biophys Res Commun, 2001, 288(1):69-74.
［11］Houten SM, Denis S, Te Brinke H,et al. Mitochondrial NADP(H) deficiency due to a mutation in NADK2 causes dienoyl-CoA reductase deficiency with hyperlysinemia［J］. Hum Mol Genet, 2014, 23(18):5009-5016.
［12］Cea M, Cagnetta A, Fulciniti M, et al. Targeting NAD+ salvage pathway induces autophagy in multiple myeloma cells via mTORC1 and extracellular signal-regulated kinase (ERK1/2) inhibition［J］. Blood, 2012, 120(17):3519-3529.