摘要
CD24(分化簇24)是一种小的重糖基化蛋白,它在许多癌症和一些癌症干细胞中过表达,并且与癌细胞的发展,侵袭和转移有关。 CD24在这些过程中的确切作用尚未完全了解,但在本文中,试图提出一系列归因于CD24的癌症相关机制。基于文献,CD24在各种癌细胞中均表达不同的信号通路,包括: Src激酶,STAT3,EGFR,Wnt /β-连环蛋白和MAPK。 Src激酶在激活p38 MAPK和STAT3途径的信号传导途径中起重要作用。 Akt和ERK是CD24激活的EGFR的下游效应物,其促进细胞增殖,侵袭和转移。 CD24通过激活NF-κB转录因子增加HER2的表达。此外,CD24通过激活Src激酶上调miR-21的表达。确定这些途径的细节以及新途径将有助于研究人员探索新的CD24靶向治疗
关键词: CD24,热稳定抗原,癌症,信号传导途径,CD24,靶向治疗。
Current Cancer Drug Targets
Title:Involvement of CD24 in Multiple Cancer Related Pathways Makes It an Interesting New Target for Cancer Therapy
Volume: 18 Issue: 4
关键词: CD24,热稳定抗原,癌症,信号传导途径,CD24,靶向治疗。
摘要: CD24 (cluster of differentiation 24) is a small heavy glycosylated protein, which is overexpressed in many cancer and some cancer stem cells and is associated with the development, invasion, and metastasis of cancer cells. The exact role of CD24 in these processes is not fully understood, however, in this article, it has been tried to present a collection of cancer-related mechanisms attributed to CD24. Based on the literature, CD24 dis-regulates different signaling pathways in various cancer cells, including; Src kinases, STAT3, EGFR, Wnt/β-catenin and MAPK. Src kinases play an important role in the signaling pathways which activate p38 MAPK and STAT3 pathways. Akt and ERK are downstream effectors of CD24-activated EGFR, which promote cell proliferation, invasion and metastasis. CD24 increases the expression of HER2 by the activation of NF-κB transcription factor. Moreover, CD24 up-regulates the expression of miR-21 oncomir through the activation of Src kinases. Identification of the details of these pathways and also new pathways will help researchers to explore new CD24 targeted therapies.
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Cite this article as:
Involvement of CD24 in Multiple Cancer Related Pathways Makes It an Interesting New Target for Cancer Therapy, Current Cancer Drug Targets 2018; 18 (4) . https://dx.doi.org/10.2174/1570163814666170818125036
DOI https://dx.doi.org/10.2174/1570163814666170818125036 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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