Fyn: a novel molecular target in prostate cancer
Fyn: a novel molecular target in prostate cancer
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发表时间：
2010
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通讯作者：
Y. Saito;A. Jensen;R. Salgia;E. Posadas
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作者：
Y. Saito;A. Jensen;R. Salgia;E. Posadas
Fyn 是 Src 激酶家族的 59 kDa 成员，历史上与发育和正常细胞生理学中的 T 细胞和神经元信号传导相关。虽然 Src 在癌症中得到了大量研究，但传统上对其他 Src 激酶（如 Fyn）的关注较少。我们的研究小组已经表明，与 Src 家族的其他成员相比，Fyn 在前列腺癌中的表达尤其上调。这表明它可能介导前列腺癌或其他恶性肿瘤中 Src 激酶的许多重要过程。这些功能不仅包括细胞生长和增殖，还包括形态发生和细胞运动。这些共同表明 Fyn 在进展和转移中发挥着关键作用。由于临床开发中的许多药物都会影响 Fyn 的激活，因此了解 Fyn 在前列腺癌和其他恶性肿瘤中可能发挥的作用对于肿瘤学可能非常重要。
Fyn is 59-kDa member of the Src family of kinases that is historically associated with T-cell and neuronal signaling in development and normal cellular physiology. While Src has been heavily studied in cancer, less attention has been traditionally awarded to the other Src kinases such as Fyn. Our group has shown that Fyn is particularly upregulated in prostate cancer in contrast to the alternative members of the Src family. This suggests that it may mediate a number of important processes attributed to Src kinases in prostate cancer or other malignancies. These functions include not only cellular growth and proliferation, but also include morphogenesis and cellular motility. These together suggest a pivotal role for Fyn in both progression and metastasis. As a number of agents in clinical development affect Fyn activation, understanding the role that Fyn may play in prostate cancer and other malignancies may be of great importance in oncology.