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DLX4 upregulates TWIST and enhances tumor migration, invasion and metastasis

Lianmei Zhang1, Manman Yang, Lin Gan

  • 1Key Laboratory of Epigenetics and Oncology, The Research Center for Preclinical Medicine, Luzhou Medical College, Luzhou 646000, China.

International Journal of Biological Sciences
|October 24, 2012
PubMed

Insights

Distal-less homeobox gene 4 (DLX4) promotes cancer metastasis by upregulating TWIST, inducing epithelial to mesenchymal transition (EMT). This study reveals DLX4

Area of Science:

  • Molecular Biology
  • Oncology
  • Gene Regulation

Background:

  • Distal-less homeobox gene 4 (DLX4) is a homeobox gene.
  • DLX4 is expressed in various cancers, including leukemia, lung, breast, ovarian, and prostate cancers.
  • The role of DLX4 in tumor metastasis is not well understood.

Purpose of the Study:

  • To investigate the molecular mechanisms by which DLX4 contributes to cancer metastasis.
  • To identify the molecular targets and pathways regulated by DLX4 in cancer cells.

Main Methods:

  • Overexpression and knockdown of DLX4 in cancer cell lines.
  • Analysis of TWIST expression using western blotting and quantitative PCR.
  • Chromatin immunoprecipitation assays to assess DLX4 binding to the TWIST gene.
  • Immunohistochemistry staining of breast tumor tissues to correlate DLX4 and TWIST expression.

Main Results:

  • Overexpression of DLX4 increased TWIST expression, promoting cancer cell migration and invasion.
  • Knockdown of DLX4 decreased TWIST expression and reduced cancer cell migration.
  • DLX4 was found to bind to regulatory regions of the TWIST gene.
  • A positive correlation between DLX4 and TWIST expression was observed in breast tumors.

Conclusions:

  • DLX4 induces epithelial to mesenchymal transition (EMT) through the upregulation of TWIST.
  • DLX4 promotes cancer cell migration, invasion, and metastasis.
  • A novel pathway involving DLX4-driven TWIST expression in promoting cancer metastasis is proposed.
Keywords:
DLX4E-CadherinTWISTbreast cancermetastasis

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