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DJ-1 upregulates breast cancer cell invasion by repressing KLF17 expression

I A Ismail1, H S Kang2, H-J Lee2

  • 11] Department of Oral Microbiology, School of Dentistry, Kyungpook National University, Daegu 700-412, Republic of Korea [2] Laboratory of Molecular Cell Biology, Department of Zoology, Faculty of Science, Assiut University, Assiut 71516, Egypt.

British Journal of Cancer
|February 8, 2014
PubMed
Abstract

Insights

DJ-1 (PARK7) promotes breast cancer invasion by downregulating KLF17 and activating the EMT pathway. This study reveals DJ-1

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • DJ-1 (PARK7) functions as an oncogene, promoting cancer cell proliferation, invasion, and metastasis.
  • The precise molecular mechanisms underlying DJ-1's role in cancer cell invasion and metastasis are not fully understood.

Purpose of the Study:

  • To elucidate the molecular mechanism by which DJ-1 enhances breast cancer cell invasion and metastasis.
  • To investigate the regulatory relationship between DJ-1 and KLF17 in breast cancer.

Main Methods:

  • Investigated DJ-1's effect on KLF17 expression using DJ-1 siRNA and overexpression in breast cancer cells.
  • Utilized luciferase reporter assays to assess DJ-1-dependent KLF17 transcriptional regulation.
  • Performed epistasis analysis to determine the functional interaction between DJ-1 and KLF17.
  • Assessed the role of Ras signaling in DJ-1-mediated cell invasion using Ras inhibitors.

Main Results:

  • DJ-1 expression is elevated in highly invasive breast cancer cells.
  • DJ-1 promotes invasion by downregulating E-cadherin and upregulating Snail, key markers of epithelial-mesenchymal transition (EMT).
  • DJ-1 overexpression reduces KLF17 mRNA and protein levels, with KLF17 acting as a direct transcriptional target.
  • KLF17 overexpression counteracted DJ-1-induced cell invasion, indicating KLF17 is a downstream mediator.
  • Ras inhibitors attenuated DJ-1-driven cell invasion, highlighting a cooperative role between DJ-1 and Ras.

Conclusions:

  • DJ-1 functions as a positive regulator of EMT in breast cancer.
  • DJ-1 promotes breast cancer cell invasion and metastasis through the KLF17/ID-1 pathway.
  • DJ-1's oncogenic activity in invasion is dependent on Ras signaling.

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