The expression and function of Frizzled-7 in human renal cell carcinoma

The expression and function of Frizzled-7 in human renal cell carcinoma
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Frizzled-7在人肾细胞癌中的表达和功能。

DOI:
10.1007/s12094-015-1362-3
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发表时间:
2016-03-01
影响因子:
3.4
通讯作者:
Zhang, L.
Zhang, L.
中科院分区:
医学4区
文献类型:
--
作者:
Xu, R.;Zeng, S.;Zhang, L.

文献摘要

被引文献

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Wnt/beta-catenin是肾细胞癌(renal cell carcinoma,RCC)发生发展的重要信号通路。Frizzled 7(Fzd 7)是Frizzled(Fzd)受体家族的一员,它与Wnt配体结合并转导经典和非经典途径。然而,Fzd 7在人肾癌中的表达研究很少。53例肾癌组织和癌旁组织收集从根治性肾切除术治疗的患者。免疫组化法检测Fzd 7的表达。将Fzd 7和GFP-shRNA分别转染肾癌细胞,免疫组化结果显示Fzd 7蛋白在肾癌组织中的表达水平明显高于癌旁组织,提示Fzd 7可能参与了肾癌的形成。Fzd 7的表达与临床病理参数无关。三种RCC细胞系:786- 0、Caki-1和OS-RC-2也表达Fzd 7。shRNA干扰Fzd 7表达后,肾癌细胞增殖轻度下降。Wnt 3a可刺激肾癌细胞增殖,但干扰Fzd 7表达后,其刺激作用减弱。Fzd 7的表达恢复导致Wnt 3a的促增殖作用恢复,提示Fzd 7可能是参与肾细胞癌形成过程的分子之一。Fzd 7可以被Wnt 3a激活以刺激细胞增殖。
Wnt/beta-catenin has emerged as an important signal pathway in renal cell carcinoma (RCC) pathogenesis. Frizzled 7 (Fzd7) is a member of Frizzled (Fzd) receptor family which binds with Wnt ligands and transduces canonical and non-canonical pathways. However, the expression of Fzd7 in human RCC is poorly investigated.53 RCC tissues and peri-tumor tissues were collected from the patients treated with radical nephrectomy. The expression of Fzd7 was investigated by immunohistochemical staining. Three RCC cells were transfected with Fzd7shRNA and GFPshRNA to investigate the function of Fzd7 in RCC cells.The immunohistochemical analysis showed that Fzd7 protein expression level was significantly increased in RCC tissues when compared with peri-tumor tissues, which suggested that Fzd7 might be involved in the formation of tumors. However, the Fzd7 expression was not correlated with clinicopathological parameters. Three RCC cell lines: 786-O, Caki-1, and OS-RC-2 also expressed Fzd7. With Fzd7 expression being interfered by shRNA, the RCC cell proliferation was mildly decreased. Wnt3a could stimulate the RCC cells proliferation, but the stimulation was decreased when Fzd7 expression was interfered. Restoring the Fzd7 expression led to the proliferation stimulation effect of Wnt3a being restored.This paper suggests that Fzd7 may act as one of the molecules that take part in the course of RCC formation. Fzd7 can be activated by Wnt3a to stimulate cell proliferation.