Related Experiment Video
Updated: Aug 5, 2026

Micromanipulation Techniques Allowing Analysis of Morphogenetic Dynamics and Turnover of Cytoskeletal Regulators
Published on: May 12, 2018
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.
Abstract:
SPIN.DOC was discovered as a transcriptional co-repressor of wingless related integration site (WNT) pathway. However, it has been found to be upregulated in various types of cancer, including hepatocellular carcinoma, colorectal cancer, renal papillary cell carcinoma. Whether SPIN.DOC functions as an oncogene or tumour suppressor gene remains uncertain. Here, we report that ectopic expression of SPIN.DOC in normal NIH3T3 fibroblast cells promotes cell proliferation, colony formation, migration and invasion. Moreover, SPIN.DOC expressing NIH3T3 cells show increased spheroid formation, suggesting enhanced stemness and transformation potential. Immunofluorescence analysis using anti-β-Tubulin suggests that SPIN.DOC may induce, formation of tubulin-based microtentacles (McTNs), indicating epithelial-to-mesenchymal (EMT) transition. In conclusion, our study helps in establishing that SPIN.DOC can function as an oncogene.
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.

