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CUB Domain-Containing Protein-1 Promotes Proliferation, Migration and Invasion in Cervical Cancer Cells

Authors Huang L, Chen Y, Lai S, Guan H, Hu X, Liu J, Zhang H, Zhang Z, Zhou J

Received 26 November 2019

Accepted for publication 27 March 2020

Published 21 May 2020 Volume 2020:12 Pages 3759—3769

DOI https://doi.org/10.2147/CMAR.S240107

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Xueqiong Zhu


Lijun Huang,1,2,* Yihong Chen,1,2,* Shuyu Lai,1 Hongmei Guan,1 Xiaoling Hu,1 Jie Liu,3 Hanrong Zhang,1 Zhenfei Zhang,1 Jueyu Zhou1

1Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, People’s Republic of China; 2The First School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, People’s Republic of China; 3Department of Gynaecology and Obstetrics, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Jueyu Zhou
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, People’s Republic of China
Tel +86-20-61648209
Fax +86-20-62789097
Email zhoujueyu@126.com

Purpose: Emerging evidence have revealed significant contributions of CUB domain-containing protein-1 (CDCP1) in tumorigenesis, including colon, renal, ovarian, pancreatic, prostate and breast cancers. However, the roles of CDCP1 in cervical cancer (CC) still remain elusive.
Materials and Methods: Quantitative reverse transcription polymerase chain reaction, immunohistochemistry and Western blotting were used to confirm the expression of CDCP1 in CC tissues compared with matched non-tumor tissues. In vitro, gain-of-function and loss-of-function studies were used to investigate the biological function and underlying mechanism of CDCP1 in cervical carcinogenesis. Furthermore, tumor growth was evaluated using a xenogenous subcutaneously implant model of CC cells in vivo.
Results: Here, we confirmed that CDCP1 was significantly increased in human CC both in mRNA and in protein levels compared to normal cervical tissues. Furthermore, we demonstrated that increased CDCP1 expression promotes proliferation, migration, invasion and mediates the epithelial-to-mesenchymal transition phenotype in HeLa and C33A cells. Also, CDCP1 knockdown reverses all the effects of enhanced CDCP1 on cell behavior in SiHa and Caski cells. Importantly, the suppressive expression of CDCP1 repressed tumor growth in a mouse xenograft model of CC.
Conclusion: In summary, our current study results provide novel insights into the role of CDCP1 in CC progression. Potentially, CDCP1 might serve as a diagnostic biomarker and a novel therapeutic target for CC.

Keywords: cervical carcinoma, CDCP1, EMT, tumor metastasis

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