SPIN.DOC induces cellular transformation of NIH3T3 normal mouse fibroblast cells

Khuraijam Mrinalini Devi1, Thangjam Davis Singh1, Rubismita Deka2

  • 1Department of Biotechnology, Manipur University, Imphal -795003, India.

Insights

SPIN.DOC, a WNT pathway regulator, promotes cancer progression. Our study shows SPIN.DOC enhances cell proliferation, migration, and stemness, establishing its role as an oncogene in cancer development.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • SPIN.DOC is a WNT pathway co-repressor.
  • SPIN.DOC is upregulated in multiple cancers.
  • Its role as an oncogene or tumor suppressor is unclear.

Purpose of the Study:

  • To investigate the function of SPIN.DOC in cancer.
  • To determine if SPIN.DOC acts as an oncogene or tumor suppressor.

Main Methods:

  • Ectopic expression of SPIN.DOC in NIH3T3 fibroblast cells.
  • Assays for cell proliferation, colony formation, migration, and invasion.
  • Spheroid formation assay to assess stemness.
  • Immunofluorescence for microtentacles (McTNs) and epithelial-to-mesenchymal transition (EMT) markers.

Main Results:

  • SPIN.DOC expression increased NIH3T3 cell proliferation, colony formation, migration, and invasion.
  • SPIN.DOC enhanced spheroid formation, indicating increased stemness.
  • SPIN.DOC expression correlated with microtentacle formation and EMT, suggesting oncogenic potential.

Conclusions:

  • SPIN.DOC functions as an oncogene.
  • SPIN.DOC promotes cancer progression through enhanced proliferation, stemness, and EMT.