Abstract
BackgroundThe molecular pathogenesis of endometrial cancer is not completely understood. CypB upregulated in many cancers, however, its role in endometrial carcinoma has not been studied. Here, we determine the effect of CypB on the growth of endometrial cancer.MethodsIn this study, we examined the expression of CypB in endometrial cancer tissues using immunohistochemistry. CypB silenced in HEC-1-B cell line by shRNA. CCK-8, colony formation assays, wound healing assays, and transwell analysis were performed to assess its effect on tumor cell proliferation and metastasis. Furthermore, microarray analysis was carried out to compare the global mRNA expression profile between the HEC-1-B and CypB-silenced HEC-1-B cells. Gene ontology and KEGG pathway enrichment analysis were performed to determine the potential function of differentially expressed genes related to CypB.ResultsWe found that CypB was upregulated in endometrial cancer, inhibit CypB expression could significantly suppress cell proliferation, metastasis, and migration. We identified 1536 differentially expressed genes related to CypB (onefold change, p < 0.05), among which 652 genes were upregulated and 884 genes were downregulated. The genes with significant difference in top were mainly enriched in the cell cycle, glycosphingolipid biosynthesis, adherens junctions, and metabolism pathways.ConclusionThe results of our study suggest that CypB may serve as a novel regulator of endometrial cell proliferation and metastasis, thus representing a novel target for gene-targeted endometrial therapy.Trial registrationYLYLLS [2018] 008. Registered 27 November 2017.
Highlights
The molecular pathogenesis of endometrial cancer is not completely understood
Cyclophilin B (CypB) expression was significantly higher in atypical complex hyperplasia and endometrial cancer tissues compared with normal endometrium tissues (Fig. 1), suggesting that higher expression of CypB is associated with the progression of endometrial cancer
Downregulation of CypB inhibits HEC-1-B cell proliferation and metastasis To investigate the role of CypB in endometrial cancer, we treated the HEC-1-B cell line with CypB-short hairpin RNA (shRNA)
Summary
The molecular pathogenesis of endometrial cancer is not completely understood. CypB upregulated in many cancers, its role in endometrial carcinoma has not been studied. Liu et al BMC Cancer (2021) 21:747 recognized as host cell receptors for the potent immunosuppressive drug cyclosporin A [7, 8]. They act as molecular chaperones that fold, translocate, and process newly synthesized proteins. Li et al using proteomics first report cyclophilin A upregulated in endometrial carcinoma serve as a potential prognostic factor [9], and up-regulation of cyclophilin A could render resistance to chemotherapeutic-induced apoptosis in cancer cells [10]. CypA been found to be up-regulated in paclitaxel-resistant endometrial cells, and knockdown of CypA could reverse the paclitaxel-resistant through suppression of MAPK kinase pathways [11]
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