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SOCS3 在非小细胞肺癌中的表达与 Pyk2 呈负相关,外源性 SOCS3 抑制 A549 细胞的增殖和侵袭。

SOCS3 expression is inversely correlated with Pyk2 in non-small cell lung cancer and exogenous SOCS3 inhibits proliferation and invasion of A549 cells.

机构信息

Department of Pathology, The First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, China.

出版信息

Pathology. 2012 Aug;44(5):434-40. doi: 10.1097/PAT.0b013e328354ffdf.

DOI:10.1097/PAT.0b013e328354ffdf
PMID:22722483
Abstract

AIMS

We have confirmed that suppressor of cytokine signalling 3 (SOCS3) is silenced and proline-rich tyrosine kinase 2 (Pyk2) is over-expressed in non-small cell lung cancer (NSCLC). The aim of this study was to investigate the correlation of SOCS3 and Pyk2 expression in NSCLC, and the effects of SOCS3 up-regulation on A549 cells.

METHODS

One hundred cases of NSCLC were detected for the expression of SOCS3 and Pyk2 by immunohistochemistry. The expression of SOCS3 and Pyk2 were also examined in human bronchial epithelial cells (HBE) and six lung cancer cell lines using Western blot and immunofluorescence staining. Then plasmid containing full-length SOCS3 was transfected into A549 cells to further investigate the effects of SOCS3 over-expression on proliferation, apoptosis and invasion of transfected cells, which were examined using MTT, flow cytometry and Transwell assays.

RESULTS

Our results showed a significant negative correlation between SOCS3 and Pyk2 in both NSCLC tissues and cell lines. Up-regulation of SOCS3 increased the apoptotic rates of transfected cells, while the numbers of proliferative and invasive cells were decreased.

CONCLUSIONS

Our data indicate that SOCS3 definitely plays roles in regulating Pyk2 expression, and up-regulation of SOCS3 could be an effective way to prevent the progression of NSCLC.

摘要

目的

我们已经证实,细胞因子信号转导抑制因子 3(SOCS3)在非小细胞肺癌(NSCLC)中被沉默,富含脯氨酸的酪氨酸激酶 2(Pyk2)过表达。本研究旨在探讨 NSCLC 中 SOCS3 和 Pyk2 表达的相关性,以及 SOCS3 上调对 A549 细胞的影响。

方法

采用免疫组织化学法检测 100 例 NSCLC 中 SOCS3 和 Pyk2 的表达。采用 Western blot 和免疫荧光染色法检测人支气管上皮细胞(HBE)和 6 种肺癌细胞系中 SOCS3 和 Pyk2 的表达。然后将含有全长 SOCS3 的质粒转染到 A549 细胞中,进一步研究 SOCS3 过表达对转染细胞增殖、凋亡和侵袭的影响,采用 MTT、流式细胞术和 Transwell 检测。

结果

我们的结果表明,SOCS3 和 Pyk2 在 NSCLC 组织和细胞系中均呈显著负相关。SOCS3 的上调增加了转染细胞的凋亡率,而增殖和侵袭细胞的数量则减少。

结论

我们的数据表明,SOCS3 确实在调节 Pyk2 表达中发挥作用,上调 SOCS3 可能是预防 NSCLC 进展的有效方法。

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