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针对细胞表面的GRP78-CD44v相互作用抑制了三阴性乳腺癌细胞中的细胞迁移

Chun-Chih Tseng^1,2,3, Pu Zhang^4,5,6, Mari B Ishak Gabra⁷

¹Department of Biochemistry and Molecular Medicine, University of Southern California, 1441 Eastlake Avenue, Los Angeles, 90089, CA, USA. charles.tseng@stjude.org.

Scientific reports

|December 20, 2025

概括

细胞表面GRP78 (78kDa葡萄糖调节蛋白) 在三阴性乳腺癌 (TNBC) 细胞中表达高. 用抗体76-E6准这种蛋白质会影响细胞形状和运动,这表明它是抗体.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
细胞生物学细胞生物学

背景情况:

三阴性乳腺癌 (TNBC) 缺乏ER,PR和HER2点,需要新的治疗策略.
细胞表面GRP78 (csGRP78),一个ER陪伴者,在癌症中被上调并参与非正规信号传递.
csGRP78是潜在的治疗点,因为它在恶性细胞上具有优先表达.

研究的目的:

研究细胞表面GRP78 (csGRP78) 在三阴性乳腺癌 (TNBC) 中的作用和治疗潜力.
探索TNBC细胞中csGRP78和CD44变异异型之间的关系.
评估用单克隆抗体76-E6.6针对csgrp78的疗效.

主要方法:

在MDA-MB-231 TNBC细胞和异种移植中表达csGRP78的特征.
对csGRP78和CD44v的免疫光共定位研究.
用抗csGRP78抗体76-E6.6.治疗TNBC细胞的方法
评估下游信号通路 (Src 激酶) 和细胞功能 (形态学,运动性).

主要成果:

超过70%的MDA-MB-231 TNBC细胞表达csgrp78,通常与细胞前部的CD44v共同定位.
在瘤外移植中,csGRP78和CD44v的同定位在体内得到证实.
针对csGRP78的抗体76-E6降低了CD44v的调节,抑制了Src激酶,改变了细胞形态和减少了细胞运动.
在GRP78上被76-E6所准的表位被映射出来.

结论:

csGRP78调节TNBC细胞形态和迁移,部分通过一个csGRP78-CD44v轴.
csGRP78代表了对三阴性乳腺癌的有希望的治疗标.
向csgrp78可能为TNBC患者提供一种新的治疗策略.

关键词:

在CD4444中,我们可以看到CD44.在 GRP78 中使用.在MDA-MB-231中使用.美国Src Src 美国TNBC电视台三阴性乳腺癌是三阴性乳腺癌.

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