Glucose-regulated protein 58 modulates β-catenin protein stability in a cervical adenocarcinoma cell line

Chia Jung Liao, Tzu I. Wu, Ya Hui Huang, Ting Chang Chang, Chyong Huey Lai, Shih Ming Jung, Chuen Hsueh, Kwang Huei Lin

研究成果: 雜誌貢獻文章同行評審

7 引文 斯高帕斯(Scopus)

摘要

Background: Cervical cancer continues to threaten women's health worldwide, and the incidence of cervical adenocarcinoma (AD) is rising in the developed countries. Previously, we showed that glucose-regulated protein 58 (Grp58) served as an independent factor predictive of poor prognosis of patients with cervical AD. However, the molecular mechanism underlying the involvement of Grp58 in cervical carcinogenesis is currently unknown.Methods: DNA microarray and enrichment analysis were used to identify the pathways disrupted by knockdown of Grp58 expression.Results: Among the pathway identified, the WNT signaling pathway was one of those that were significantly associated with knockdown of Grp58 expression in HeLa cells. Our experiments showed that β-catenin, a critical effector of WNT signaling, was stabilized thereby accumulated in stable Grp58 knockdown cells. Membrane localization of β-catenin was observed in Grp58 knockdown, but not control cells. Using a transwell assay, we found that accumulated β-catenin induced by Grp58 knockdown or lithium chloride treatment inhibited the migration ability of HeLa cells. Furthermore, an inverse expression pattern of Grp58 and β-catenin was observed in cervical tissues.Conclusions: Our results demonstrate that β-catenin stability is negatively regulated by Grp58 in HeLa cells. Overexpression of Grp58 may be responsible for the loss of or decrease in membranous β-catenin expression in cervical AD.

原文英語
文章編號555
期刊BMC Cancer
14
發行號1
DOIs
出版狀態已發佈 - 八月 1 2014

ASJC Scopus subject areas

  • 腫瘤科
  • 遺傳學
  • 癌症研究

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