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Jing X, Wu H, Ji X, et al. Cortactin promotes cell migration and invasion through upregulation of the dedicator of cytokinesis 1 expression in human colorectal cancer. Oncol Rep. 2016;36(4):1946-1952doi: 10.3892/or.2016.5058.
Jing, X., Wu, H., Ji, X., Wu, H., Shi, M., & Zhao, R. (2016). Cortactin promotes cell migration and invasion through upregulation of the dedicator of cytokinesis 1 expression in human colorectal cancer. Oncology reports, 36(4), 1946-1952. https://doi.org/10.3892/or.2016.5058
Jing, Xiaoqian, et al. "Cortactin promotes cell migration and invasion through upregulation of the dedicator of cytokinesis 1 expression in human colorectal cancer." Oncology reports vol. 36,4 (2016): 1946-1952. doi: https://doi.org/10.3892/or.2016.5058
Jing X, Wu H, Ji X, Wu H, Shi M, Zhao R. Cortactin promotes cell migration and invasion through upregulation of the dedicator of cytokinesis 1 expression in human colorectal cancer. Oncol Rep. 2016 Oct;36(4):1946-1952. doi: 10.3892/or.2016.5058. Epub 2016 Aug 31. PMID: 27633051.
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Oncol Rep. 2016 Oct;36(4):1946-1952. doi: 10.3892/or.2016.5058. Epub 2016 Aug 31.

Cortactin promotes cell migration and invasion through upregulation of the dedicator of cytokinesis 1 expression in human colorectal cancer.

Oncology reports

Xiaoqian Jing, Huo Wu, Xiaopin Ji, Haoxuan Wu, Minmin Shi, Ren Zhao

Affiliations

  1. Department of Surgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.

PMID: 27633051 DOI: 10.3892/or.2016.5058

Abstract

Cortactin (CTTN), a major substrate of the Src tyrosine kinase, has been implicated in cell proliferation, motility and invasion in various types of cancer. However, the molecular mechanisms of CTTN-driven malignant behavior remain unclear. In the current study, we determined the expression of CTTN in colorectal cancer and investigated its underlying mechanism in the metastasis of colorectal cancer. We confirmed increased CTTN expression in lymph node-positive CRC specimens and highly invasive CRC cell lines. Further study has shown that overexpression of CTTN promoted CRC cell migration and invasion, whereas CTTN silencing inhibited CRC cell migratory and invasive capacities in vitro. Mechanistically, CTTN increases expression of dedicator of cytokinesis 1 (DOCK1) and gene silencing of DOCK1 partially abolishes the migration and invasion capacity by CTTN. Our findings indicate that CTTN promotes metastasis of CRC cells by increasing DOCK1 expression and this could offer a promising therapeutic target for colorectal cancer treatment.

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