期刊文献+

Imbalanced expression of mitogen-activated protein kinase phosphatase-1 and phosphorylated extracellular signal-regulated kinases in lung squamous cell carcinoma 被引量:2

Imbalanced expression of mitogen-activated protein kinase phosphatase-1 and phosphorylated extracellular signal-regulated kinases in lung squamous cell carcinoma
原文传递
导出
摘要 Objective: Mitogen-activated protein kinases (MAPKs) are correlated with a more malignant phenotype in many cancers. This study was designed to evaluate the predictive value of the expression of MAPK phosphatase-1 (MKP-1) and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERKl/2), as the key regulatory mechanism of the MAPKs, in lung squamous cell carcinoma (SCC). Methods: We assessed the expressions of MKP-1 and p-ERK1/2 in twenty subjects at different differentiation degree of SCC and five normal lungs by immunohistochemistry and real-time reverse transcriptase polymerase chain reaction (RT-PCR) analysis. Results: Immunohistochemistry and real-time RT-PCR assay showed that the expression of MKP-1 was gradually decreased as tissue type went from normal lung tissues to increasingly undifferentiated carcinoma, and it was negatively correlated with tumor differentiation (P〈0.01). However, the expression of p-ERK1/2 or ERKl/2 was gradually increased as tissue type went from normal lung tissues to increasingly undifferentiated carcinoma, and it was positively correlated with tumor differentiation (P〈0.01). Conclusions: Our data indicates the relevance of MKP-1 and p-ERK1/2 in SCC as a potential positive and negative prognostic factor. The imbalanced expression of MKP-1 and p-ERKl/2 may play a role in the development of SCC and these two molecules may be new targets for the therapy and prognosis of SCC. Objective:Mitogen-activated protein kinases (MAPKs) are correlated with a more malignant phenotype in many cancers.This study was designed to evaluate the predictive value of the expression of MAPK phosphatase-1 (MKP-1) and phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK 1/2),as the key regulatory mechanism of the MAPKs,in lung squamous cell carcinoma (SCC).Methods:We assessed the expressions of MKP-1 and p-ERK 1/2 in twenty subjects at different differentiation degree of SCC and five normal lungs by immunohistochemistry and real-time reverse transcriptase polymerase chain reaction (RT-PCR) analysis.Results:Immunohistochemistry and real-time RT-PCR assay showed that the expression of MKP-1 was gradually decreased as tissue type went from normal lung tissues to increasingly undifferentiated carcinoma,and it was negatively correlated with tumor differentiation (P<0.01).However,the expression of p-ERK 1/2 or ERK 1/2 was gradually increased as tissue type went from normal lung tissues to increasingly undifferentiated carcinoma,and it was positively correlated with tumor differentiation (P<0.01).Conclusions:Our data indicates the relevance of MKP-1 and p-ERK 1/2 in SCC as a potential positive and negative prognostic factor.The imbalanced expression of MKP-1 and p-ERK 1/2 may play a role in the development of SCC and these two molecules may be new targets for the therapy and prognosis of SCC.
出处 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2011年第10期828-834,共7页 浙江大学学报(英文版)B辑(生物医学与生物技术)
基金 supported by the National Natural Science Foundation of China (No. 30900654) the Science and Technology Department of Zhejiang Province (No. 2009R10031) the Health Bureau of Zhejiang Province (No. 2009QN010), China
关键词 Mitogen-activated protein kinase phosphatase-1 (MKP-1) Extracellular signal-regulated kinase (ERK) Lung squamous cell carcinoma (SCC) Prognostic factor 激活 Mitogen 的蛋白质 kinase phosphatase-1 (MKP-1 ) ;细胞外的调整信号的 kinase (英皇家空军之阶级最低之兵) ;肺有鳞的房间癌(SCC ) ;预示的因素
  • 相关文献

参考文献32

  • 1Adeyinka, A., Nui, Y., Cherlet, T., Snell, L., Watson, P.H., Murphy, L.C., 2002. Activated mitogen-activated protein kinase expression during human breast tumorigenesis and breast cancer progression. Clin. Cancer Res., 8(6): 1747-1753.
  • 2Bermudez, O., Pages, G., Gimond, C., 2010. The dual- specificity MAP kinase phosphatases: critical roles in development and cancer. Am. J. Physiol. Cell Physiol., 299(2):C189-C202. [doi:10.1152/ajpcoll.00347.2009].
  • 3Blackball, F.H., Pintilie, M., Michael, M., Leighl, N., Feld, R., Tsao, M.S., Shepherd, F.A., 2003. Expression and prog- nostic significance of kit, protein kinase B, and mitogen- activated protein kinase in patients with small cell lung cancer. Clin. Cancer Res., 9(6):2241-2247.
  • 4Bogoyevitch, M.A., 2006. The isoform-specific functions of the c-Jun N-terminal kinases (JNKs): differences revealed by gene targeting. Bioessays, 28(9):923-934. [doi:10. 1002/bies.20458].
  • 5Bogoyevitch, M.A., Arthur, P.G., 2008. Irthibitors of c-Jun N-terminal kinases: JuNK no more? Biochim. Biophys. Acta, 1784(1):76-93. [doi: 10.1016/j.bbapap.2007.09.013].
  • 6Chang, L.F., Karin, M., 2001. Mammalian MAP kinase sig- nalling cascades. Nature, 410(6824):37-40. [doi:10. 1038/35065000].
  • 7Chen, H., Zhu, G., Li, Y., Padia, R.N., Dong, Z., Pan, Z.K., Liu, K., Huang, S., 2009. Extracellular signal-regulated kinase signaling pathway regulates breast cancer cell migration by maintaining slug expression. Cancer Res., 69(24): 9228-9235. [doi:10.1158/0008-5472.CAN-09-1950].
  • 8Denkert; C., Schrnitt, W.D., Berger, S., Reles, A., Pest, S., Siegert, A., Lichtenegger, W., Dietel, M., Hauptmann, S., 2002. Expression of mitogen-activated protein kinase phosphatase-1 (MKP-1) in primary human ovarian car- cinoma. Int. J. Cancer, 102(5):507-513. [doi:10.1002/ ijc. 10746].
  • 9Dickinson, R.J., Keyse, S.M., 2006. Diverse physiological functions for dual-specificity MAP kinase phosphatases. J. Cell Sci., 119(22):4607-4615. [doi:50.1242/jes.03266].
  • 10Dunn, K.L., Espino, P.S., Drobic, B., He, S., Davie, J.R., 2003. The Ras-MAPK signal transduction pathway, cancer and chromatin remodeling. Biochem. Cell Biol., 83(1):1-14. [doi:10.1139/o04-121].

同被引文献17

引证文献2

二级引证文献17

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部