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Updated: Feb 19, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
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Epithelial‑mesenchymal transition in colorectal carcinoma cells is mediated by DEK/IMP3

Shuping You1, Yun Guan2, Weihong Li1

  • 1Department of Anorectal Surgery, Jingmen No. 2 People's Hospital, Jingmen, Hubei 448000, P.R. China.

Molecular Medicine Reports
|November 9, 2017
PubMed

Insights

DEK silencing inhibits epithelial-mesenchymal transition (EMT) in colorectal cancer cells, reducing viability and invasion while increasing apoptosis. This suggests DEK is a potential therapeutic target for colorectal carcinoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Colorectal carcinoma (CRC) is a significant global health concern.
  • Epithelial-mesenchymal transition (EMT) is a key process in cancer progression and metastasis.
  • The role of DEK proto-oncogene (DEK) and insulin-like growth factor II mRNA binding protein 3 (IMP3) in CRC-associated EMT requires further elucidation.

Purpose of the Study:

  • To investigate the inhibitory effects of DEK/IMP3 on EMT in colorectal carcinoma cells.
  • To determine the impact of DEK knockdown on cell viability, apoptosis, and invasion.
  • To analyze the expression of EMT markers (E-cadherin, vimentin, MMP-9) following DEK silencing.

Main Methods:

  • Utilized human colorectal cancer cell lines (SW620 and SW480).
  • Employed lentivirus-mediated transfection for DEK knockdown.
  • Assessed cell viability (MTT assay), apoptosis (flow cytometry), and invasion (Transwell assay).
  • Quantified gene and protein expression of E-cadherin, vimentin, and MMP-9 (qPCR and Western blot).

Main Results:

  • DEK knockdown significantly reduced cell viability and increased apoptosis in CRC cells.
  • Silencing DEK led to a significant elevation in E-cadherin expression.
  • DEK interference markedly decreased the expression of vimentin and matrix metalloproteinase-9 (MMP-9).

Conclusions:

  • DEK plays a role in mediating EMT in colorectal carcinoma cells.
  • DEK silencing impacts the invasive potential of CRC cells.
  • Targeting DEK offers a potential therapeutic strategy for colorectal carcinoma by affecting proliferation, apoptosis, and EMT.

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