Knockdown of PKM2 suppresses tumor progression in human cervical cancer by modulating epithelial–mesenchymal transition via Wnt/β-catenin signaling
Authors Lin Y, Meng F, Lu Z, Chen K, Tao Y, Ouyang Y, Cao X
Received 25 June 2018
Accepted for publication 9 August 2018
Published 4 October 2018 Volume 2018:10 Pages 4191—4202
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Antonella D'Anneo
Yanzhu Lin,1,* Fanqing Meng,2,* Zhiyuan Lu,3 Kai Chen,1 Yalan Tao,1 Yi Ouyang,1 Xinping Cao1
1Department of Radiation Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China; 2Department of Anesthesiology, Jinan Maternity and Child Care Hospital, Jinan, China; 3Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
*These authors contributed equally to this work
Background: Pyruvate kinase isozyme type M2 (PKM2) is a key glycolytic enzyme and is upregulated in multiple human malignancies. However, the role of PKM2 in human cervical cancer (CC) remains elusive. Thus, this study explored the role of PKM2 in CC by detecting its expression patterns in human CC tissues and cell lines and investigated its effects on cell proliferation and invasion.
Materials and methods: Quantitative reverse transcription polymerase chain reaction (qRT-PCR), immunohistochemistry and western blotting assays were used to detect the expression of PKM2 in CC tissues and CC cells. In vitro, we overexpressed and knocked down PKM2 expression in CC cell lines and investigated the biological function and underlying mechanism of PKM2 in cervical carcinogenesis.
Results: The results showed that PKM2 mRNA and protein were highly expressed in CC tissues and cell lines. Furthermore, increasing PKM2 expression was closely correlated with the clinical stage (P=0.001) and lymph node metastasis (P=0.023). The functional roles of PKM2 were determined using Cell Counting Kit-8, colony formation, and transwell assays. The results showed that PKM2 knockdown inhibited cell proliferation and the migratory and invasive capacities of CC cells, suppressed epithelial–mesenchymal transition (EMT), and inhibited Wnt/β-catenin signaling in vitro. However, overexpression of PKM2 led to increased proliferation and invasion activity as well as the EMT in CC cells.
Conclusion: Taken together, our study results revealed that PKM2 may act as a molecular target for CC treatment.
Keywords: Cervical cancer, PKM2, invasion, epithelial–mesenchymal transition, migration
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]