Open AccessEpithelial‑mesenchymal transition in colorectal carcinoma cells is mediated by DEK/IMP3
Author(s) -
You Shang,
Yun Guan,
Weihong Li
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.7943
Subject(s) - vimentin , epithelial–mesenchymal transition , viability assay , apoptosis , transfection , flow cytometry , gene silencing , biology , cell growth , gene knockdown , microbiology and biotechnology , cancer research , cell culture , oncogene , small interfering rna , chemistry , cell cycle , cancer , immunology , metastasis , immunohistochemistry , biochemistry , genetics , gene
To investigate the inhibitory effects of DEK/insulin‑like growth factor II mRNA binding protein 3 (IMP3) on epithelial‑mesenchymal transition (EMT) in colorectal carcinoma cells. SW620 and SW480 cell lines were selected. DEK‑interfering lentivirus was transfected to knockdown DEK expression. Subsequently, MTT assays and flow cytometry were utilized to measure cell viability, and apoptosis, respectively. Cell invasion was detected using a Transwell assay. Quantitative polymerase chain reaction and western blot analysis were used to detect the expression of E‑cadherin, vimentin, and matrix metalloproteinase (MMP)‑9. Compared with the blank control, cells transfected with DEK‑interfering lentivirus demonstrated a remarkable reduction in cell viability (P<0.05). The apoptotic rate in the DEK‑interfering lentivirus group was significantly enhanced compared with the blank control group (P<0.05). In the DEK‑interfering lentivirus group, the expression of E‑cadherin was significantly elevated (P<0.05), while the expression of vimentin and MMP‑9 were significantly reduced in both cell lines (P<0.05). The results of the present study demonstrated that EMT of colorectal carcinoma cells was partially mediated by DEK, which likely affected the invasive ability of colorectal carcinoma cells. In addition, cell proliferation and apoptosis were susceptible to DEK silencing. The current study has provided experimental evidence for the treatment of colorectal carcinoma using DEK silencing.