DPY30 regulates cervical squamous cell carcinoma by mediating epithelial–mesenchymal transition (EMT)
Feng-xi He,1,* Li-li Zhang,1,* Peng-fei Jin,1 Dan-dan Liu,2 Ai-hua Li11Department of Obstetrics and Gynecology, Liaocheng People’s Hospital Affiliated to Shandong First Medical University, Liaocheng 252000, People’s Republic of China; 2Shandong First Medical University, Taian 271...
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doaj-c59c1e2e09614a669417e97951bf30882020-11-25T02:25:57ZengDove Medical PressOncoTargets and Therapy1178-69302019-09-01Volume 127139714748302DPY30 regulates cervical squamous cell carcinoma by mediating epithelial–mesenchymal transition (EMT)He FZhang LJin PLiu DLi AFeng-xi He,1,* Li-li Zhang,1,* Peng-fei Jin,1 Dan-dan Liu,2 Ai-hua Li11Department of Obstetrics and Gynecology, Liaocheng People’s Hospital Affiliated to Shandong First Medical University, Liaocheng 252000, People’s Republic of China; 2Shandong First Medical University, Taian 271016, People’s Republic of China *These authors contributed equally to this work Correspondence: Ai-hua LiDepartment of Obstetrics and Gynecology, Liaocheng People’s Hospital Affiliated to Shandong First Medical University, No. 67 Dongchang West Road, Liaocheng City, Shandong Province 252000, People’s Republic of ChinaTel +86 1 356 205 0087Email weiran0228@163.comIntroduction: Set1/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.Methods: We 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.Results: Immunohistochemical 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.Conclusion: Our results suggest that elevated DPY30 levels may contribute to EMT by activating Wnt/β-catenin signaling in the progression of CSCC.Keywords: DPY30, cervical squamous cell carcinoma, epithelial–mesenchymal transition, Wnt/β-catenin pathwayhttps://www.dovepress.com/dpy30-regulates-cervical-squamous-cell-carcinoma-by-mediating-epitheli-peer-reviewed-article-OTTDPY30cervical squamous cell carcinomaepithelial–mesenchymal transitionWnt/β-catenin pathway |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
He F Zhang L Jin P Liu D Li A |
spellingShingle |
He F Zhang L Jin P Liu D Li A DPY30 regulates cervical squamous cell carcinoma by mediating epithelial–mesenchymal transition (EMT) OncoTargets and Therapy DPY30 cervical squamous cell carcinoma epithelial–mesenchymal transition Wnt/β-catenin pathway |
author_facet |
He F Zhang L Jin P Liu D Li A |
author_sort |
He F |
title |
DPY30 regulates cervical squamous cell carcinoma by mediating epithelial–mesenchymal transition (EMT) |
title_short |
DPY30 regulates cervical squamous cell carcinoma by mediating epithelial–mesenchymal transition (EMT) |
title_full |
DPY30 regulates cervical squamous cell carcinoma by mediating epithelial–mesenchymal transition (EMT) |
title_fullStr |
DPY30 regulates cervical squamous cell carcinoma by mediating epithelial–mesenchymal transition (EMT) |
title_full_unstemmed |
DPY30 regulates cervical squamous cell carcinoma by mediating epithelial–mesenchymal transition (EMT) |
title_sort |
dpy30 regulates cervical squamous cell carcinoma by mediating epithelial–mesenchymal transition (emt) |
publisher |
Dove Medical Press |
series |
OncoTargets and Therapy |
issn |
1178-6930 |
publishDate |
2019-09-01 |
description |
Feng-xi He,1,* Li-li Zhang,1,* Peng-fei Jin,1 Dan-dan Liu,2 Ai-hua Li11Department of Obstetrics and Gynecology, Liaocheng People’s Hospital Affiliated to Shandong First Medical University, Liaocheng 252000, People’s Republic of China; 2Shandong First Medical University, Taian 271016, People’s Republic of China *These authors contributed equally to this work Correspondence: Ai-hua LiDepartment of Obstetrics and Gynecology, Liaocheng People’s Hospital Affiliated to Shandong First Medical University, No. 67 Dongchang West Road, Liaocheng City, Shandong Province 252000, People’s Republic of ChinaTel +86 1 356 205 0087Email weiran0228@163.comIntroduction: Set1/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.Methods: We 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.Results: Immunohistochemical 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.Conclusion: Our results suggest that elevated DPY30 levels may contribute to EMT by activating Wnt/β-catenin signaling in the progression of CSCC.Keywords: DPY30, cervical squamous cell carcinoma, epithelial–mesenchymal transition, Wnt/β-catenin pathway |
topic |
DPY30 cervical squamous cell carcinoma epithelial–mesenchymal transition Wnt/β-catenin pathway |
url |
https://www.dovepress.com/dpy30-regulates-cervical-squamous-cell-carcinoma-by-mediating-epitheli-peer-reviewed-article-OTT |
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