N-Linked Glycan Branching and Fucosylation Are Increased Directly in Hcc Tissue As Determined through in Situ Glycan Imaging.
N-Linked Glycan Branching and Fucosylation Are Increased Directly in Hcc Tissue As Determined through in Situ Glycan Imaging.
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DOI：
10.1021/acs.jproteome.8b00323
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发表时间：
2018-10-05
影响因子：
4.4
通讯作者：
Mehta AS
中科院分区：
文献类型：
--
作者：
West CA;Wang M;Herrera H;Liang H;Black A;Angel PM;Drake RR;Mehta AS
肝细胞癌 (HCC) 仍然是世界上第五大常见癌症，每年导致超过 70 万人死亡。长期以来，血清糖基化的变化与这种癌症有关，但该物质的来源尚不清楚，并且对 HCC 组织的直接聚糖分析也受到限制。我们的实验室之前开发了一种基于 N 连接聚糖成像的原位组织方法，无需在分析前对组织进行显微切割和溶解。我们使用这种方法分析了 138 个 HCC 组织样本，并将癌组织中的 N 连接聚糖与邻近的未转化组织或肝硬化但无癌症患者的组织进行了比较。与肝硬化或邻近组织相比，在 HCC 组织中发现 10 种聚糖显着升高。这些聚糖分为两大类，一类是岩藻糖基化水平增加的聚糖，另一类是分支水平增加的、有或没有任何岩藻糖修饰的聚糖。此外，岩藻糖基化糖型水平的增加与生存时间的缩短有关。这项工作支持这样的假设：HCC 血清中岩藻糖基化 N 连接聚糖水平的增加是直接由癌症组织产生的。
Hepatocellular carcinoma (HCC) remains as the fifth most common cancer in the world and accounts for more than 700,000 deaths annually. Changes in serum glycosylation have long been associated with this cancer but the source of that material is unknown and direct glycan analysis of HCC tissues has been limited. Our laboratory previously developed a method of in situ tissue based N-linked glycan imaging that bypasses the need for microdissection and solubilization of tissue prior to analysis. We used this methodology in the analysis of 138 HCC tissue samples and compared the N-linked glycans in cancer tissue with either adjacent untransformed or tissue from patients with liver cirrhosis but no cancer. Ten glycans were found significantly elevated in HCC tissues as compared to cirrhotic or adjacent tissue. These glycans fell into two major classes, those with increased levels of fucosylation and those with increased levels of branching with or without any fucose modifications. In addition, increased levels of fucosylated glycoforms were associated with a reduction in survival time. This work supports the hypothesis that the increased levels of fucosylated N-linked glycans in HCC serum are produced directly from the cancer tissue.
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影响因子：
3.7
作者：
Furukawa J;Tsuda M;Okada K;Kimura T;Piao J;Tanaka S;Shinohara Y
通讯作者：
Shinohara Y
影响因子：
11.4
作者：
BOLSCHER, JGM;VANDERBIJL, MMW;PLOEGH, HL
通讯作者：
PLOEGH, HL
影响因子：
3.7
作者：
Houser J;Kozmon S;Mishra D;Mishra SK;Romano PR;Wimmerová M;Koča J
通讯作者：
Koča J
DOI：
10.3233/cbm-2010-0190
发表时间：
2010
期刊：
Cancer biomarkers : section A of Disease markers
影响因子：
--
作者：
Hann HW;Wang M;Hafner J;Long RE;Kim SH;Ahn M;Park S;Comunale MA;Block TM;Mehta A
通讯作者：
Mehta A
影响因子：
64.5
作者：
Cancer Genome Atlas Research Network. Electronic address: wheeler@bcm.edu;Cancer Genome Atlas Research Network
通讯作者：
Cancer Genome Atlas Research Network