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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >CD98hc (SLC3A2) mediates integrin signaling.
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CD98hc (SLC3A2) mediates integrin signaling.

机译：CD98hc（SLC3A2）介导整联蛋白信号传导。

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摘要

Integrins regulate cellular behaviors through signaling pathways, including Rho GTPases and kinases. CD98 heterodimers, comprised of a heavy chain (CD98hc, SLC3A2) and one of several light chains, interact with integrins through CD98hc. CD98hc overexpression leads to anchorage-independent cell growth and tumorigenesis in 3T3 fibroblasts and activates certain integrin-regulated signaling pathways. To establish the biological function of CD98hc, we disrupted the gene and analyzed CD98hc-null cells. Here we report that CD98hc contributes to integrin-dependent cell spreading, cell migration, and protection from apoptosis. Furthermore, CD98hc is required for efficient adhesion-induced activation of Akt and Rac GTPase, major contributors to the integrin-dependent signals involved in cell survival and cell migration. CD98 promotes amino acid transport through its light chains; however, a CD98hc mutant that interacts with beta1 integrins, but not CD98 light chains, restored integrin-dependent signaling and protection from apoptosis. beta1 integrins are involved in the pathogenesis of certain cancers. CD98hc deletion markedly impaired the ability of embryonic stem cells to form teratocarcinomas in mice; teratocarcinoma formation was reconstituted by reexpression of CD98hc or of the mutant that interacts exclusively with integrins. Thus, CD98hc is an integrin-associated protein that mediates integrin-dependent signals, which promote tumorigenesis.
机译：整联蛋白通过信号途径调节细胞行为，包括Rho GTPases和激酶。由重链（CD98hc，SLC3A2）和几条轻链之一组成的CD98异二聚体通过CD98hc与整联蛋白相互作用。 CD98hc的过表达导致3T3成纤维细胞中不依赖贴壁的细胞生长和肿瘤发生，并激活某些整联蛋白调节的信号通路。为了建立CD98hc的生物学功能，我们破坏了该基因并分析了CD98hc-null细胞。在这里，我们报告CD98hc有助于整合素依赖性细胞的扩散，细胞迁移和凋亡的保护。此外，CD98hc是Akt和Rac GTPase的有效粘附诱导激活所必需的，Akt和Rac GTPase是参与细胞存活和细胞迁移的整联蛋白依赖性信号的主要贡献者。 CD98通过其轻链促进氨基酸运输；但是，与beta1整合素，但不与CD98轻链相互作用的CD98hc突变体恢复了整合素依赖性信号传导并防止凋亡。 beta1整合素与某些癌症的发病机制有关。 CD98hc的缺失显着损害了小鼠胚胎干细胞形成畸胎瘤的能力。通过重新表达CD98hc或仅与整联蛋白相互作用的突变体可以重建畸胎瘤的形成。因此，CD98hc是一种整合素相关蛋白，可介导整合素依赖性信号，从而促进肿瘤发生。

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