DcR3 induces epithelial-mesenchymal transition through activation of the TGF-β3/SMAD signaling pathway in CRC

Yan-Ping Liu1,2,3, Hui-Fang Zhu1,2,3, Ding-Li Liu4

  • 1Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Oncotarget
|October 21, 2016
PubMed

Insights

Decoy receptor 3 (DcR3) promotes colorectal cancer (CRC) growth and metastasis by activating TGF-β3/SMAD-mediated epithelial-mesenchymal transition (EMT). Elevated DcR3 levels indicate poor prognosis in CRC patients, suggesting its potential as a biomarker.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Decoy receptor 3 (DcR3), a tumor necrosis factor receptor (TNFR) family member, is implicated in tumorigenesis.
  • The specific role of DcR3 in human colorectal cancer (CRC) remains unclear.

Purpose of the Study:

  • To investigate the role of DcR3 in the development and progression of human colorectal cancer (CRC).
  • To explore DcR3 as a potential prognostic biomarker for CRC.

Main Methods:

  • Quantitative analysis of DcR3 expression in CRC tissues versus normal tissues.
  • In vitro and in vivo experiments assessing the effects of DcR3 overexpression and knockdown on CRC cell behavior.
  • Investigation of DcR3's functional role in TGF-β3/SMAD-mediated epithelial-mesenchymal transition (EMT).

Main Results:

  • DcR3 expression is significantly upregulated in CRC tissues and correlates with invasion, metastasis, and poor prognosis.
  • DcR3 overexpression enhances CRC cell proliferation, migration, and tumorigenesis, while knockdown inhibits these processes.
  • DcR3 is crucial for TGF-β3/SMAD-mediated EMT in CRC cells, and its cooperation with related proteins predicts patient survival.

Conclusions:

  • DcR3 facilitates CRC development and metastasis through TGF-β3/SMAD-mediated EMT.
  • DcR3 serves as a potential prognostic biomarker for colorectal cancer.

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