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CXCL12-CXCR4在人类恶性肿瘤中的生物学功能 被引量:2

Biological Functions of CXCL12-CXCR4 in Human Malignant Tumors
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摘要 转移和细胞浸润是实体癌和淋巴癌治疗的难点,也是疾病复发和死亡的主要原因。癌细胞的迁移是肿瘤转移和侵袭的前提。CXCL12-CXCR4通路在实体瘤和白血病的发病中发挥重要作用。CXCL12与其受体CXCR4之间的相互作用可以激活多种信号通路,调节不同的生理和病理生理过程。因此,阻断CXCL12-CXCR4的结合和/或下游通路在治疗各种疾病和癌症方面具有临床益处。目前,已发现一些CXCL12和CXCR4拮抗剂,并通过研究证实其在抗肿瘤活性方面取得了令人鼓舞的结果;但这些药物由于其严重的毒副作用未能大规模应用于临床患者。迫切需要研发新型CXCL12-CXCR4轴拮抗剂以治疗肿瘤。本文综述了CXCR4通路在实体肿瘤和白血病中的最新研究进展,并讨论了CXCR4通路在实体肿瘤和白血病中的治疗价值和未来的研究方向。 Metastasis and cell infiltration are the difficulties in the treatment of solid and lymphatic carcinoma and the main causes of disease recurrence and death.The migration of cancer cells is a prerequisite for tumor metastasis and invasion.The CXCL12-CXCR4 pathway plays an important role in the pathogenesis of solid tumors and leukemia.The interaction between CXCL12 and its receptor CXCR4 can activate multiple signaling pathways and regulate different physiological and pathophysiological processes.Thus,blocking CXCL12-CXCR4 binding and/or downstream pathways has clinical benefits in treating a variety of diseases and cancers.Although some CXCL12 and CXCR4 antagonists have been identified and have shown encouraging results in terms of antitumor activity,these drugs have not been widely used in clinical patients due to their serious toxic and side effects.There is an urgent need to develop novel CXCL12-CXCR4 axis antagonists for the treatment of tumors.Herein,we review the recent research progress of CXCR4 pathway in solid tumors and leukemia,and discuss the therapeutic value and future research direction of CXCR4 pathways in solid tumors and leukemia.
作者 王森 落继先 Istvan Boldogh WANG Sen;LUO Ji-Xian;Istvan Boldogh(School of Life Sciences,Shanxi University,Taiyuan 030006,China;Department of Microbiology and Immunology,University of Texas Medical Branch at Galveston,Galveston TX 77555,USA)
出处 《中国生物化学与分子生物学报》 CAS CSCD 北大核心 2022年第5期577-586,共10页 Chinese Journal of Biochemistry and Molecular Biology
基金 国家自然科学基金项目(No.31401216) 山西省回国留学人员科研资助项目(No.2017-012) 山西省自然科学基金(No.201901D111010)资助。
关键词 趋化因子受体4 趋化因子配体12 癌症 白血病 通路 C-X-C chemokine receptor 4(CXCR4) C-X-C motif ligand 12(CXCL12) cancer leukemia pathways
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  • 1Magda Kucia,Kacper Jankowski,Ryan Reca,Marcin Wysoczynski,Laura Bandura,Daniel J. Allendorf,Jin Zhang,Janina Ratajczak,Mariusz Z. Ratajczak.CXCR4–SDF-1 Signalling, Locomotion, Chemotaxis and Adhesion[J].The Histochemical Journal.2004(3) 被引量:1
  • 2Andreeva AV,Kutuzov MA,Voyno-Yasenetskaya TA.Scaffolding proteins in G-protein signaling[].J Mol Signal.2007 被引量:1
  • 3Chang HH,Kuo MY,Cheng SJ,Chiang CP.Expression of BCL10 is significantly associated with the progression and prognosis of oral squamous cell carcinomas in Taiwan[].Oral Oncology.2008 被引量:1
  • 4Grabiner BC,Blonska M,Lin PC,You Y,Wang D,Sun J, et al.CARMA3 deficiency abrogates G protein-coupled receptor-induced NF-κB activation[].Genes and Development.2007 被引量:1
  • 5Klemm S,Zimmermann S,Peschel C,Mak TW,Ruland J.Bcl10 and Malt1 control lysophosphatidic acid-induced NF-kappaB activation and cytokine production[].Proceedings of the National Academy of Sciences of the United States of America.2007 被引量:1
  • 6Martin D,Galisteo R,Gutkind JS.CXCL8/IL8 stimulates vascular endothelial growth factor (VEGF) expression and the autocrine activation of VEGFR2 in endothelial cells by activating NFkappaB through the CBM (Carma3/Bcl10/Malt1) complex[].Journal of Biological Chemistry.2009 被引量:1
  • 7Nagasawa T,Nakajima T,Tachibana K,Iizasa H,Bleul CC,Yoshie O, et al.Molecular cloning and charac- terization of a murine pre-B-cell growth-stimulating factor/stromal cell-derived factor 1 receptor, a murine homolog of the human immunodeficiency virus 1 entry coreceptor fusin[].Proceedings of the National Academy of Sciences of the United States of America.1996 被引量:1
  • 8Santiskulvong C,Rozengurt E.Protein kinase Calpha mediates feedback inhibition of EGF receptor transactivation induced by Gq-coupled receptor agonists[].Cellular Signalling.2007 被引量:1
  • 9Sun Y,McGarrigle D,Huang XY.When a Gprotein-coupled receptor does not couple to a G protein[].Mol Biosyst.2007 被引量:1
  • 10Wang D,Matsumoto R,You Y,Che T,Lin XY,Gaffen SL, et al.CD3/CD28 costimulation-induced NF- kappaB activation is mediated by recruitment of protein kinase C-theta, Bcl10, and IkappaB kinase beta to the immunological synapse through CARMA1[].Molecular and Cellular Biology.2004 被引量:1

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