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本文引用的文献

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Examining galectin binding specificity using glycan microarrays.使用聚糖微阵列检测半乳糖凝集素结合特异性。
Methods Mol Biol. 2015;1207:115-31. doi: 10.1007/978-1-4939-1396-1_8.
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Evolving mechanistic insights into galectin functions.对半乳糖凝集素功能的机制洞察不断深入。
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Immature truncated O-glycophenotype of cancer directly induces oncogenic features.癌症不成熟的截短型O-糖表型直接诱导致癌特征。
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C1GALT1 promotes invasive phenotypes of hepatocellular carcinoma cells by modulating integrin β1 glycosylation and activity.C1GALT1通过调节整合素β1的糖基化和活性促进肝癌细胞的侵袭表型。
PLoS One. 2014 Aug 4;9(8):e94995. doi: 10.1371/journal.pone.0094995. eCollection 2014.
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Microbial glycan microarrays define key features of host-microbial interactions.微生物聚糖微阵列定义了宿主-微生物相互作用的关键特征。
Nat Chem Biol. 2014 Jun;10(6):470-6. doi: 10.1038/nchembio.1525. Epub 2014 May 11.
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C1GALT1 overexpression promotes the invasive behavior of colon cancer cells through modifying O-glycosylation of FGFR2.C1GALT1过表达通过修饰FGFR2的O-糖基化促进结肠癌细胞的侵袭行为。
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The Cosmc connection to the Tn antigen in cancer.癌症中Cosmc与Tn抗原的联系。
Cancer Biomark. 2014 Jan 1;14(1):63-81. doi: 10.3233/CBM-130375.
8
Elevated levels of glycosylphosphatidylinositol (GPI) anchored proteins in plasma from human cancers detected by C. septicum alpha toxin.通过败血梭菌α毒素检测到人类癌症患者血浆中糖基磷脂酰肌醇(GPI)锚定蛋白水平升高。
Cancer Biomark. 2014 Jan 1;14(1):55-62. doi: 10.3233/CBM-130377.
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Identification of a novel protein binding motif within the T-synthase for the molecular chaperone Cosmc.鉴定 T 合成酶中分子伴侣 Cosmc 的新型蛋白结合基序。
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Involvement of a non-human sialic Acid in human cancer.一种非人类唾液酸在人类癌症中的作用。
Front Oncol. 2014 Feb 19;4:33. doi: 10.3389/fonc.2014.00033. eCollection 2014.

癌症中的蛋白质糖基化

Protein glycosylation in cancer.

作者信息

Stowell Sean R, Ju Tongzhong, Cummings Richard D

机构信息

Departments of 1Pathology and Laboratory Medicine and.

出版信息

Annu Rev Pathol. 2015;10:473-510. doi: 10.1146/annurev-pathol-012414-040438.

DOI:10.1146/annurev-pathol-012414-040438
PMID:25621663
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4396820/
Abstract

Neoplastic transformation results in a wide variety of cellular alterations that impact the growth, survival, and general behavior of affected tissue. Although genetic alterations underpin the development of neoplastic disease, epigenetic changes can exert an equally significant effect on neoplastic transformation. Among neoplasia-associated epigenetic alterations, changes in cellular glycosylation have recently received attention as a key component of neoplastic progression. Alterations in glycosylation appear to not only directly impact cell growth and survival but also facilitate tumor-induced immunomodulation and eventual metastasis. Many of these changes may support neoplastic progression, and unique alterations in tumor-associated glycosylation may also serve as a distinct feature of cancer cells and therefore provide novel diagnostic and even therapeutic targets.

摘要

肿瘤转化会导致多种细胞改变,这些改变会影响受影响组织的生长、存活及一般行为。虽然基因改变是肿瘤性疾病发展的基础,但表观遗传变化对肿瘤转化也可产生同样显著的影响。在与肿瘤形成相关的表观遗传改变中,细胞糖基化的变化最近作为肿瘤进展的关键组成部分受到关注。糖基化的改变似乎不仅直接影响细胞生长和存活,还促进肿瘤诱导的免疫调节及最终的转移。这些变化中的许多可能支持肿瘤进展,肿瘤相关糖基化的独特改变也可能作为癌细胞的一个显著特征,从而提供新的诊断甚至治疗靶点。