Upregulation of interleukin‑17F in colorectal cancer promotes tumor invasion by inducing epithelial‑mesenchymal transition | Zendy

Yusheng Chen | Zendy; Yang Zhou | Zendy; Dejun Wu | Zendy; Zhijun Min | Zendy; Yingjun Quan | Zendy

Open Access

Upregulation of interleukin‑17F in colorectal cancer promotes tumor invasion by inducing epithelial‑mesenchymal transition

Author(s) -

Yusheng Chen,

Yang Zhou,

Dejun Wu,

Zhijun Min,

Yingjun Quan

Publication year - 2019

Publication title -

oncology reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.094

H-Index - 96

eISSN - 1791-2431

pISSN - 1021-335X

DOI - 10.3892/or.2019.7220

Subject(s) - oncogene , epithelial–mesenchymal transition , colorectal cancer , molecular medicine , cancer research , cell cycle , downregulation and upregulation , cancer , cell , interleukin , proinflammatory cytokine , interleukin 8 , biology , medicine , metastasis , immunology , cytokine , inflammation , gene , biochemistry , genetics

Interleukin‑17F (IL‑17F) is a member of the IL‑17 family of proteins. Previous studies concerning IL‑17F have mainly focused on its proinflammatory responses, whereas the present study explored its role as an oncogene in colorectal cancer (CRC). The present study investigated the expression of IL‑17F in 69 patients with CRC. IL‑17F was significantly overexpressed in tumor mucosa compared with that in the paired non‑tumor mucosa. Furthermore, several studies from Gene Expression Omnibus (GEO) databases were analyzed to assess the association between IL‑17F and overall survival and relapse‑free survival time. Recombinant human IL‑17F protein (rhIL‑17F) and anti‑IL‑17F antibody were used to study the effect of IL‑17F on the CRC cell line HCT‑116 in vitro. According to the results of Transwell and wound healing assays, rhIL‑17F promoted HCT‑116 cell migration and invasion which was mediated by inducing epithelial‑mesenchymal transition (EMT), whereas anti‑IL‑17F inhibited EMT.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research