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用单克隆抗体进行的CD44s靶向治疗可阻断9L胶质肉瘤的脑内侵袭和生长。

CD44s-targeted treatment with monoclonal antibody blocks intracerebral invasion and growth of 9L gliosarcoma.

作者信息

Gunia S, Hussein S, Radu D L, Pütz K M, Breyer R, Hecker H, Samii M, Walter G F, Stan A C

机构信息

Institute of Neuropathology, Hannover Medical School, Germany.

出版信息

Clin Exp Metastasis. 1999 May;17(3):221-30. doi: 10.1023/a:1006699203287.

Abstract

Glioma invasiveness is a complex process involving recognition and attachment of tumor cells to particular extracellular matrix (ECM) molecules prior to migrating into proteolytically modified matrix and inducing angiogenesis. CD44 is a group of transmembrane adhesion molecules found on a wide variety of cells including gliomas that has been suggested as the principal mediator of migration/invasion. The aim of the present study was to demonstrate whether antibody specific for the standard form of CD44 (CD44s, 85-90 kDa) might prevent invasion, thus blocking growth of the 9L gliosarcoma in vivo. High expression of CD44s on the surface of 9L cells and brain tumors was demonstrated by immunochemistry. Fluorescence-activated cell sorting (FACS) demonstrated binding saturation of anti-CD44s monoclonal antibody (mAb) to the receptor at 1 microg/5 x 10(5) cells. Blocking of CD44s in vitro resulted in a dose-dependent progressive, up to 95%+/-2.5% detachment of 9L cells from ECM-coated culture surfaces. Blocking of CD44s in vivo resulted in significantly reduced 9L brain tumors (2.5%+/-0.4%)--measured as the quotient: tumor surface (mm2)/brain surface (mm2) x 100--as compared to untreated (16.1%+/-2.2%) or sham-treated rats (16%+/-3.7% to 16.1%+/-3%). We conclude that CD44s-targeted treatment with specific mAb may be an effective means for preventing glioma progression.

摘要

胶质瘤侵袭是一个复杂的过程,涉及肿瘤细胞在迁移到经蛋白水解修饰的基质并诱导血管生成之前,识别并附着于特定的细胞外基质(ECM)分子。CD44是一类跨膜黏附分子,存在于包括胶质瘤在内的多种细胞上,被认为是迁移/侵袭的主要介质。本研究的目的是证明针对标准形式CD44(CD44s,85 - 90 kDa)的抗体是否可以预防侵袭,从而在体内阻断9L胶质肉瘤的生长。免疫化学证明9L细胞和脑肿瘤表面存在高表达的CD44s。荧光激活细胞分选(FACS)表明,抗CD44s单克隆抗体(mAb)与受体的结合饱和度为1 μg/5×10⁵个细胞。体外阻断CD44s导致9L细胞从ECM包被的培养表面呈剂量依赖性逐渐脱离,最高可达95%±2.5%。与未治疗(16.1%±2.2%)或假治疗大鼠(16%±3.7%至16.1%±3%)相比,体内阻断CD44s导致9L脑肿瘤显著减少(2.5%±0.4%),以肿瘤表面积(mm²)/脑表面积(mm²)×100的商来衡量。我们得出结论,用特异性mAb靶向治疗CD44s可能是预防胶质瘤进展的有效手段。

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