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Trefoil factor-2, human spasmolytic polypeptide, promotes branching morphogenesis in MCF-7 cells

E N Lalani1, R Williams, Y Jayaram

  • 1Department of Histopathology, Imperial College of Science, Technology and Medicine, Hammersmith Hospital, London, United Kingdom.

Insights

Trefoil factor 2 (TFF2) promotes cell survival by inhibiting apoptosis and acts as a morphogen in breast cancer cells, complementing TFF1's role in cell motility.

Area of Science:

  • Cell biology
  • Molecular biology
  • Cancer research

Background:

  • Trefoil factor (TFF) family members are implicated in epithelial repair and cancer.
  • TFF1 and TFF3 influence cell motility and growth suppression.
  • The in vivo role of TFF2, often co-expressed with TFF1 in gastric epithelia, remains largely undefined.

Purpose of the Study:

  • To investigate the effects of TFF2 on epithelial and mesenchymal cell proliferation and morphogenesis.
  • To elucidate the specific mechanisms by which TFF2 influences cell behavior.

Main Methods:

  • Cell proliferation assays across various epithelial and mesenchymal cell lines.
  • Morphogenesis assays using type I collagen lattices with MCF-7 breast carcinoma cells.
  • Analysis of cell motility via videomicroscopy.
  • Assessment of apoptosis using trypan blue exclusion and DNA fragmentation ELISA.

Main Results:

  • TFF2 did not affect the proliferation of any tested cell lines.
  • Low concentrations of TFF2 induced complex branching morphogenesis in MCF-7 cells within collagen lattices over 14-42 days.
  • This morphogenic effect was dependent on the presence of TFF1 and abolished by specific antibodies.
  • TFF2 inhibited apoptosis in MCF-7 cells by approximately 30%, promoting cell survival.
  • TFF2 did not influence cell motility in MCF-7 cells, unlike TFF1.

Conclusions:

  • TFF2 functions as a morphogen in specific contexts, notably in breast carcinoma cells (MCF-7), particularly when TFF1 is present.
  • TFF2 promotes cell survival by inhibiting apoptosis, suggesting a complementary role to TFF1's motogenic effects.
  • These findings offer insights into the differential roles of TFF family members in epithelial repair and neoplastic processes.

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