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Area of Science:

  • Oncology
  • Biophysics
  • Cell Biology

Background:

  • The tumor microenvironment (TME) features altered biophysical forces, including interstitial fluid flow (IFF), which can impact cancer progression.
  • IFF, the movement of fluid through tissue, is known to promote cancer cell invasion, but the underlying signaling pathways are not fully understood.

Purpose of the Study:

  • To elucidate the signaling cascades activated by IFF that mediate invasion in ERBB2/HER2-expressing breast cancer cells.
  • To investigate the role of epithelial-to-mesenchymal transition (EMT) in modulating the cellular response to IFF-induced invasion.

Main Methods:

  • Investigated IFF-induced invasion in ERBB2-expressing breast cancer cells, including those with constitutive or TGFβ1-induced EMT.
  • Utilized inhibitors and genetic manipulation to assess the roles of phosphoinositide-3-kinase (PI3K) subunits (p110α, p110β), chemokine receptor CXCR4, and its ligand CXCL12.

Main Results:

  • IFF induces invasion of ERBB2-expressing breast cancer cells via PI3K activation.
  • In EMT-activated cells, IFF-mediated invasion requires CXCR4, CXCL12, and PI3K subunits p110α and p110β.
  • In wild-type cells, IFF-induced invasion is independent of CXCR4 and relies solely on p110α.
  • EMT induction in wild-type cells renders IFF-induced invasion dependent on CXCR4 and p110β.

Conclusions:

  • Identified a novel signaling mechanism where IFF induces invasion in ERBB2-expressing breast cancer cells through a CXCR4-PI3K pathway, contingent on EMT status.
  • The cellular response to IFF is dependent on the EMT state and malignancy of the cancer cells, highlighting potential therapeutic targets.