ArticleMolecular biology research communications2025
SPIN.DOC induces cellular transformation of NIH3T3 normal mouse fibroblast cells.
Article in Molecular biology research communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
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.
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