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肝再生磷酸酶基因家族在非小细胞肺癌中的表达改变。

Altered expression of phosphatase of regenerating liver gene family in non-small cell lung cancer.

机构信息

Graduate School of Medical Science and Engineering, Biomedical Research Center, KAIST Institute for the BioCentury, Korea Advanced Institute of Science and Technology, and Department of Thoracic and Cardiovascular Surgery, Eulji University Hospital, Daejeon 305-701, Republic of Korea.

出版信息

Oncol Rep. 2012 Feb;27(2):535-40. doi: 10.3892/or.2011.1495. Epub 2011 Oct 6.

Abstract

Protein tyrosine phophatases (PTPs) are implicated in the tumorigenesis and metastasis of human cancer. The phosphatase of regenerating liver (PRL) gene family, a subgroup of PTPs is also linked to these processes. In many solid cancers, high levels of PRL-3 expression are related with metastasis and poor prognosis. However, the expression patterns of PRL-1 and -2 have not been explored in lung cancer yet. Thus, we investigated the expression levels of PRL-1, -2 and -3 in the tissues of primary lung cancer patients. The protein expression levels of PRL-2, but not PRL-1 and -3 were increased in cancer tissues. However, there was no correlation between mRNA and protein expression levels of the PRLs. Reporter assays showed that PRLs suppressed the activity of the p21 promoter but promoted AP-1 activity. Furthermore, transfection of PRLs showed significantly increased cell proliferation. Therefore, these results suggest that PRL-2 plays an important role in lung cancer and can be a biomarker of lung cancer, substituting for the function of other PRLs.

摘要

蛋白酪氨酸磷酸酶(PTPs)参与人类癌症的发生和转移。肝再生磷酸酶(PRL)基因家族是 PTPs 的一个亚群,也与这些过程有关。在许多实体瘤中,PRL-3 的高表达与转移和预后不良有关。然而,PRL-1 和 -2 的表达模式在肺癌中尚未得到探索。因此,我们研究了 PRL-1、-2 和 -3 在原发性肺癌患者组织中的表达水平。PRL-2 的蛋白表达水平在癌组织中增加,而 PRL-1 和 -3 则没有增加。然而,PRLs 的 mRNA 和蛋白表达水平之间没有相关性。报告基因检测表明,PRLs 抑制 p21 启动子的活性,但促进 AP-1 活性。此外,PRLs 的转染显示细胞增殖明显增加。因此,这些结果表明 PRL-2 在肺癌中发挥重要作用,可以作为肺癌的生物标志物,替代其他 PRLs 的功能。

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