DPY30 regulates cervical squamous cell carcinoma by mediating epithelial-mesenchymal transition (EMT).

Abstract

IntroductionSet1/MLL complexes are the main histone H3K4 methyltransferases and are crucial regulators of tumor pathogenesis. DPY30 is a fairly uncharacterized protein in the Set1/MLL complex, but it has been reported to regulate tumor growth. However, the exact mechanism by which DPY30 mediates the progression of cervical squamous cell carcinoma (CSCC) remains unknown. In the present study, we investigated the role of DPY30 in CSCC at a molecular level.MethodsWe obtained normal cervical and cervical cancer tissue samples from patients. We used immunohistochemistry and real-time polymerase chain reaction (PCR) to detect DPY30 expression in CSCC tissues. In addition, we used the human cervical cancer cell line to evaluate expression levels of DPY30 and epithelial–mesenchymal transition (EMT) markers in vitro.ResultsImmunohistochemical and real-time PCR analyses showed that DPY30 expression was upregulated in tissue samples from patients with CSCC and that DPY30 levels were associated with EMT markers such as E-cadherin. Furthermore, knock-down of DPY30 by siRNA resulted in a decrease in the proliferation, migration, and invasion of CSCC cells. We also found that DPY30-induced EMT is mediated by the Wnt/β-catenin signaling pathway.ConclusionOur results suggest that elevated DPY30 levels may contribute to EMT by activating Wnt/β-catenin signaling in the progression of CSCC.