Mucins and toll-like receptors: kith and kin in infection and cancer.
Mucins and toll-like receptors: kith and kin in infection and cancer.
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DOI：
10.1016/j.canlet.2012.01.040
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发表时间：
2012-08-28
期刊：
影响因子：
9.7
通讯作者：
Batra, Surinder K.
中科院分区：
文献类型：
--
作者：
Tarang, Shikha;Kumar, Sushil;Batra, Surinder K.
炎症是感染和癌症中常见的潜在生物现象。粘蛋白是糖蛋白，它为异物通过上皮表面的不良进入建立物理屏障。已知在许多癌症中粘蛋白的表达失调和异常糖基化模式。 TLR 是一类受体，可识别入侵病原体的分子模式并激活复杂的炎症途径以清除它们。在许多癌症中观察到 TLR 的异常表达。粘蛋白和 TLR 的高度协调作用是进化良好的宿主防御机制；然而，两者在其他非传染性疾病中的联系却很少受到关注。在这里，我们概述了粘蛋白和 TLR 如何为宿主提供保护并在致癌过程中解除管制。此外，我们提出了它们在癌症发病机制中交叉调节的可能机制。由于粘蛋白和 TLR 都是治疗上重要的一类分子，因此了解连接两者的潜在分子机制将为癌症治疗靶向开辟新途径。
Inflammation is underlying biological phenomenon common in infection and cancer. Mucins are glycoproteins which establish a physical barrier for undesirable entry of foreign materials through epithelial surfaces. A deregulated expression and an anomalous glycosylation pattern of mucins are known in large number of cancers. TLRs are class of receptors which recognize the molecular patterns of invading pathogens and activate complex inflammatory pathways to clear them. Aberrant expression of TLRs is observed in many cancers. A highly orchestrated action of mucins and TLRs is well evolved host defence mechanism; however, a link between the two in other non-infectious conditions has received less attention. Here we present an overview as to how mucins and TLRs give protection to the host and are deregulated during carcinogenesis. Further, we propose the possible mechanisms of cross-regulation between them in pathogenesis of cancer. As both mucins and TLRs are therapeutically important class of molecules, an understanding of the underlying molecular mechanisms connecting the two will open new avenues for the therapeutic targeting of cancer.
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影响因子：
3.2
作者：
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