Abstract
BackgroundCervical 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.MethodsDNA microarray and enrichment analysis were used to identify the pathways disrupted by knockdown of Grp58 expression.ResultsAmong 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.ConclusionsOur 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.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2407-14-555) contains supplementary material, which is available to authorized users.
Highlights
Cervical cancer continues to threaten women’s health worldwide, and the incidence of cervical adenocarcinoma (AD) is rising in the developed countries
We explored the role of glucose-regulated protein 58 (Grp58) in cervical AD progression and the molecular mechanism underlying Grp58 function
Altered WNT signaling pathway in Grp58-knockdown HeLa cells Previously, we used an Affymetrix microarray to identify the genes disrupted upon knockdown of Grp58 expression [4]
Summary
Cervical cancer continues to threaten women’s health worldwide, and the incidence of cervical adenocarcinoma (AD) is rising in the developed countries. We showed that glucose-regulated protein 58 (Grp58) served as an independent factor predictive of poor prognosis of patients with cervical AD. The molecular mechanism underlying the involvement of Grp in cervical carcinogenesis is currently unknown. HPV alone is not sufficient to cause cervical cancer; other molecular markers of cervical carcinogenesis are essential. We demonstrated that glucoseregulated protein 58 (Grp58) serves as an independent prognostic factor for cervical AD, but not SCC [4]. We explored the role of Grp in cervical AD progression and the molecular mechanism underlying Grp function
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