SPARC: a matricellular regulator of tumorigenesis.
SPARC: a matricellular regulator of tumorigenesis.
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DOI：
10.1007/s12079-009-0072-4
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发表时间：
2009-12
影响因子：
4.1
通讯作者：
Brekken RA
中科院分区：
文献类型：
--
作者：
Arnold SA;Brekken RA
尽管许多临床研究发现SPARC表达与恶性进展和患者生存相关，但SPARC在肿瘤发生和转移中的功能机制仍然难以捉摸。 SPARC 的活性依赖于环境和细胞类型，这一点在临床相关研究和动物模型中都显示出 SPARC 对肿瘤进展看似矛盾的影响这一事实。 SPARC 决定致瘤表型的能力归因于其对整合素和生长因子/趋化因子的生物利用度和信号传导的影响。这些分子途径导致许多影响恶性进展的生理事件，包括细胞外基质重塑、血管生成、免疫调节和转移。鉴于 SPARC 具有如此多样的活性，本综述全面介绍了 SPARC 在人类癌症和小鼠模型中的不同作用，并描述了 SPARC 介导这些作用的潜在机制。我们的目标是深入了解 SPARC 等基质细胞蛋白如何产生矛盾但相关的肿瘤结果，以便统一明显不一致的科学文献集。
Although many clinical studies have found a correlation of SPARC expression with malignant progression and patient survival, the mechanisms for SPARC function in tumorigenesis and metastasis remain elusive. The activity of SPARC is context- and cell-type-dependent, which is highlighted by the fact that SPARC has shown seemingly contradictory effects on tumor progression in both clinical correlative studies and in animal models. The capacity of SPARC to dictate tumorigenic phenotype has been attributed to its effects on the bioavailability and signaling of integrins and growth factors/chemokines. These molecular pathways contribute to many physiological events affecting malignant progression, including extracellular matrix remodeling, angiogenesis, immune modulation and metastasis. Given that SPARC is credited with such varied activities, this review presents a comprehensive account of the divergent effects of SPARC in human cancers and mouse models, as well as a description of the potential mechanisms by which SPARC mediates these effects. We aim to provide insight into how a matricellular protein such as SPARC might generate paradoxical, yet relevant, tumor outcomes in order to unify an apparently incongruent collection of scientific literature.
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影响因子：
15.9
作者：
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通讯作者：
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