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SRC induces podoplanin expression to promote cell migration

Yongquan Shen1, Chen-Shan Chen2, Hitoshi Ichikawa3

  • 1Molecular Biology Department, Stratford, New Jersey 08084.

The Journal of Biological Chemistry
|February 4, 2010
PubMed

Insights

Normal cells can reverse cancer traits through contact normalization. This study reveals podoplanin (Pdpn) is key to tumor cell migration and is suppressed by normal cells, offering new cancer targets.

Area of Science:

  • Cell Biology
  • Cancer Research
  • Molecular Biology

Background:

  • Nontransformed cells can revert tumor cells to a normal state via contact normalization.
  • Mechanisms of contact normalization, crucial for preventing cancer invasion, remain poorly understood.
  • Tumor cell migration is essential for malignancy and metastasis.

Purpose of the Study:

  • To identify genes regulated by contact normalization in Src-transformed cells.
  • To elucidate the role of Src signaling in tumor cell migration and invasion.
  • To understand how normal cells suppress tumor-promoting phenotypes.

Main Methods:

  • Gene expression analysis in Src-transformed and nontransformed cells.
  • Investigating the role of Crk-associated substrate (Cas) in Src signaling.
  • Analyzing podoplanin (Pdpn) expression and its impact on cell migration.

Main Results:

  • Src-transformed cells exhibit increased migration, partly due to induced podoplanin (Pdpn) expression.
  • Podoplanin (Pdpn) is identified as a key mediator of tumor cell migration induced by Src.
  • Nontransformed cells suppress Pdpn expression in adjacent Src-transformed cells, reversing migratory phenotypes.
  • Pdpn was among 23 genes upregulated by Src and downregulated by contact normalization.
  • 16 genes, including growth factor receptors, were downregulated by Src and upregulated by contact normalization.

Conclusions:

  • Podoplanin (Pdpn) is a critical mediator of Src-driven tumor cell migration and invasion.
  • Contact normalization by nontransformed cells suppresses Pdpn expression, inhibiting tumor cell migration.
  • Identification of Pdpn and other regulated genes provides potential therapeutic targets for cancer invasion and metastasis.

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