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DEAD-box helicase 27 plays a tumor-promoter role by regulating the stem cell-like activity of human colorectal cancer cells

Authors Yang C, Li D, Bai Y, Song S, Yan P, Wu R, Zhang Y, Hu G, Lin C, Li X, Huang L

Received 13 October 2018

Accepted for publication 7 December 2018

Published 28 December 2018 Volume 2019:12 Pages 233—241


Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Andrew Yee

Peer reviewer comments 2

Editor who approved publication: Dr Takuya Aoki

Chunxing Yang,1,* Daojiang Li,1,* Yang Bai,1 Shenglei Song,1 Peicheng Yan,1 Runliu Wu,1 Yi Zhang,1 Gui Hu,1 Changwei Lin,1 Xiaorong Li,1 Lihuang Huang2

1Department of Gastrointestinal Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China; 2Department of Central laboratory, The Third Xiangya Hospital of Central South University, Changsha, Hunan Province, China

*These authors contributed equally to this work

Background: Cancer stem cells (CSCs) are responsible for all important characteristics of tumors. DEAD-box helicase 27 (DDX27) is a member of the DEAD-box RNA helicase family, and there have been only a few studies on DDX27 function in cancer cells. This study is aimed at exploring whether DDX27 has any relation to tumorigenesis of colorectal cancer (CRC) and elucidating the potential mechanism.
Methods: Data from Catalog Of Somatic Mutations In Cancer, Gene Expression Omnibus, and The Cancer Genome Atlas databases reveal that DDX27 is overexpressed in CRC tissues. qRT-PCR and Western blots were used to evaluate the expression level of DDX27 in 40 paired clinical CRC samples. DDX27 was knockdown in HT29 and HCT116 cell line with shRNA. Then CCK-8, colony formation assay and flow cytometry assay were performed to examine proliferative ability, cell cycle and sensitivity to 5-fluorouracil. Sphere-formation assay and in vivo subcutaneous tumor-formation assay were used to assess self-renewal in vitro and vivo as well as the tumor-initiating potential.
Results: DDX27 is upregulated in CRC tissues and downregulation of DDX27 inhibits proliferation of colorectal cancer cell and promotes sensitivity to 5-fluorouracil. Downregulation of DDX27 can downregulate the gene expression of known CSC markers in CRC cells, inhibit sphere-formation ability, and promote colonosphere differentiation. Downregulation of DDX27 in CSCs can decrease the tumor-initiating ability of CRC cells in vivo.
Conclusion: DDX27 may play a tumorpromoter role of CRC by regulating the stem cell-like activity of CRC cells.

Keywords: DDX27, cancer stem cell, colonosphere, tumor-initiating ability

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