Hypersialylation in Cancer: Modulation of Inflammation and Therapeutic Opportunities.
Hypersialylation in Cancer: Modulation of Inflammation and Therapeutic Opportunities.
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DOI：
10.3390/cancers10060207
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发表时间：
2018-06-18
期刊：
影响因子：
5.2
通讯作者：
Macauley MS
中科院分区：
文献类型：
--
作者：
Rodrigues E;Macauley MS
细胞表面糖基化是动态的，经常在生理或病理生理条件下随着细胞分化而改变。肿瘤细胞上的糖基化改变正受到人们的关注，因为它广泛存在于各种癌症类型中，最近的研究证明了异常糖基化在推动癌症不同阶段进展中的功能作用。糖基化的一个变化可能与癌症分期和疾病预后相关，那就是高唾液酸化。唾液酸水平升高在癌症中普遍存在，越来越多的证据表明，超唾液酸化对癌细胞有利，特别是从调节免疫细胞反应的角度。唾液酸结合受体，如Siglecs和选择素，处于很好的位置，可以被癌症过度唾液酸化利用。越来越多的证据表明，Siglecs调节肿瘤微环境中的关键免疫细胞类型，特别是那些负责维持适当炎症环境的细胞。这些研究带来了新的创新方法来阻断超唾液酸化的影响，方法是直接减少癌细胞上的唾液酸，或者阻断唾液酸与Siglecs或选择素之间的相互作用。在这里，我们回顾了最近研究癌细胞如何过度唾液酸化、如何使癌细胞和肿瘤受益的工作，并提出了消除癌症过度唾液酸化的治疗方法。
Cell surface glycosylation is dynamic and often changes in response to cellular differentiation under physiological or pathophysiological conditions. Altered glycosylation on cancers cells is gaining attention due its wide-spread occurrence across a variety of cancer types and recent studies that have documented functional roles for aberrant glycosylation in driving cancer progression at various stages. One change in glycosylation that can correlate with cancer stage and disease prognosis is hypersialylation. Increased levels of sialic acid are pervasive in cancer and a growing body of evidence demonstrates how hypersialylation is advantageous to cancer cells, particularly from the perspective of modulating immune cell responses. Sialic acid-binding receptors, such as Siglecs and Selectins, are well-positioned to be exploited by cancer hypersialylation. Evidence is also mounting that Siglecs modulate key immune cell types in the tumor microenvironment, particularly those responsible for maintaining the appropriate inflammatory environment. From these studies have come new and innovative ways to block the effects of hypersialylation by directly reducing sialic acid on cancer cells or blocking interactions between sialic acid and Siglecs or Selectins. Here we review recent works examining how cancer cells become hypersialylated, how hypersialylation benefits cancer cells and tumors, and proposed therapies to abrogate hypersialylation of cancer.
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影响因子：
4.3
作者：
Borsig L
通讯作者：
Borsig L
影响因子：
4.3
作者：
Angata, Takashi;Tabuchi, Yukako;Nakamura, Mitsuru
通讯作者：
Nakamura, Mitsuru
影响因子：
11.2
作者：
Bull, Christian;Boltje, Thomas J.;Adema, Gosse J.
通讯作者：
Adema, Gosse J.
粘蛋白MUC1通过参与凝集素SIGLEC-9调节肿瘤免疫学微环境。
影响因子：
30.5
作者：
Beatson R;Tajadura-Ortega V;Achkova D;Picco G;Tsourouktsoglou TD;Klausing S;Hillier M;Maher J;Noll T;Crocker PR;Taylor-Papadimitriou J;Burchell JM
通讯作者：
Burchell JM
影响因子：
6.6
作者：
Carrascal, Mylene A.;Severino, Paulo F.;Videira, Paula A.
通讯作者：
Videira, Paula A.