Proteomic analysis on N, N'-dinitrosopiperazine-mediated metastasis of nasopharyngeal carcinoma 6-10B cells.
Proteomic analysis on N, N'-dinitrosopiperazine-mediated metastasis of nasopharyngeal carcinoma 6-10B cells.
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DOI：
10.1186/1471-2091-13-25
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发表时间：
2012-11-19
期刊：
影响因子：
--
通讯作者：
Tang F
中科院分区：
文献类型：
--
作者：
Li Y;Liu N;Huang D;Zhang Z;Peng Z;Duan C;Tang X;Tan G;Yan G;Mei W;Tang F
鼻咽癌（Nasopharyngeal carcinoma，NPC）具有高度转移的特点。N，N′-二亚硝基哌嗪（DNP）参与了鼻咽癌的转移，但其机制尚不清楚。本研究的目的是揭示DNP参与转移的发病机制。本研究以鼻咽癌细胞系SUNE-1的低转移细胞株6- 10 B为研究对象，探讨DNP介导鼻咽癌转移的机制。6- 10 B细胞在含有2 H 4-L-赖氨酸和13 C 6 15 N 4-L-精氨酸或常规L-赖氨酸和L-精氨酸的DMEM中生长，并通过基质辅助激光解吸/电离飞行时间质谱法鉴定氨基酸的掺入。 用0 - 18 μM DNP处理标记的6- 10 B细胞，以确定非细胞毒性浓度（NCC）范围。NCC为0 - 10 μM。在此范围内用DNP处理后，在体外检测细胞的运动和侵袭，并在裸鼠中证实DNP介导的转移。DNP在体内外均能增加6- 10 B细胞的转移。使用定量蛋白质组学研究DNP诱导的蛋白质表达。基于SILAC的方法定量了2698种蛋白质，其中371种在DNP处理后显示出显著变化（172种上调和199种下调蛋白质）。DNP诱导线粒体蛋白质丰度的变化，介导氧化应激状态和氧化还原状态的失衡，增加细胞骨架蛋白、组织蛋白酶、前梯度-2和clusterin的表达。DNP还可增加分泌型AKR 1 B10、组织蛋白酶B和clusterin 6- 10 B细胞的表达。基因本体论和免疫途径分析表明，DNP可能通过调节蛋白质合成、细胞运动、脂质代谢、分子转运、细胞生长和增殖等信号通路。DNP可能通过调节细胞骨架蛋白、组织蛋白酶、前梯度蛋白-2和聚集蛋白的表达，增强鼻咽癌细胞的运动性和侵袭性，参与鼻咽癌的转移。
Nasopharyngeal carcinoma (NPC) has a high metastatic feature. N,N′-Dinitrosopiperazine (DNP) is involved in NPC metastasis, but its mechanism is not clear. The aim of this study is to reveal the pathogenesis of DNP-involved metastasis. 6-10B cells with low metastasis are from NPC cell line SUNE-1, were used to investigate the mechanism of DNP-mediated NPC metastasis. 6-10B cells were grown in DMEM containing 2H4-L-lysine and 13C 6 15 N4-L-arginine or conventional L-lysine and L-arginine, and identified the incorporation of amino acid by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Labeled 6-10B cells were treated with DNP at 0 -18 μM to establish the non-cytotoxic concentration (NCC) range. NCC was 0 -10 μM. Following treatment with DNP at this range, the motility and invasion of cells were detected in vitro, and DNP-mediated metastasis was confirmed in the nude mice. DNP increased 6-10B cell metastasis in vitro and vivo. DNP-induced protein expression was investigated using a quantitative proteomic. The SILAC-based approach quantified 2698 proteins, 371 of which showed significant change after DNP treatment (172 up-regulated and 199 down-regulated proteins). DNP induced the change in abundance of mitochondrial proteins, mediated the status of oxidative stress and the imbalance of redox state, increased cytoskeletal protein, cathepsin, anterior gradient-2, and clusterin expression. DNP also increased the expression of secretory AKR1B10, cathepsin B and clusterin 6-10B cells. Gene Ontology and Ingenuity Pathway analysis showed that DNP may regulate protein synthesis, cellular movement, lipid metabolism, molecular transport, cellular growth and proliferation signaling pathways. DNP may regulate cytoskeletal protein, cathepsin, anterior gradient-2, and clusterin expression, increase NPC cells motility and invasion, is involved NPC metastasis.
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影响因子：
6.7
作者：
Kong QL;Hu LJ;Cao JY;Huang YJ;Xu LH;Liang Y;Xiong D;Guan S;Guo BH;Mai HQ;Chen QY;Zhang X;Li MZ;Shao JY;Qian CN;Xia YF;Song LB;Zeng YX;Zeng MS
通讯作者：
Zeng MS
影响因子：
3.6
作者：
Paksoy, Mustafa;Hardal, Umit;Caglar, Cakar
通讯作者：
Caglar, Cakar
影响因子：
3.8
作者：
Jia WH;Luo XY;Feng BJ;Ruan HL;Bei JX;Liu WS;Qin HD;Feng QS;Chen LZ;Yao SY;Zeng YX
通讯作者：
Zeng YX
DOI：
10.1007/s00432-007-0264-3
发表时间：
2008-02-01
影响因子：
3.6
作者：
del Casar, Jose M.;Corte, Maria D.;Vizoso, Francisco J.
通讯作者：
Vizoso, Francisco J.
影响因子：
7
作者：
Olsen, JV;de Godoy, LMF;Mann, M
通讯作者：
Mann, M