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
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
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
This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.Download Article [PDF] View Full Text [HTML][Machine readable]