Conversely, when silencing S100A4 by shRNA technology, a dramatic decrease in tumor development of the pancreatic MIA PaCa-2 cell line was observed.

[9] S100A4 is highly associated with components of the cytoskeleton and when this gene is upregulated, it changes the cell’s morphology, making it more susceptible to invasion from proteins, such as cathepsin B and cyclin B1, that contribute to metastasis.

Experimental knockout therapy data have suggested that S100A4 exhibits a form of control over cathepsin B and cyclin B1, and that suppressing it can reduce the invasive capabilities of PGCCs and their daughter cells.

Studies on invasive breast cancer have found that S100A4 plays a major role in high-density collagen deposition, which is one of the clinical symptoms of tumor metastasis.

Significantly higher levels of S100A4 were found in samples that exhibited lymph node metastasis than in those that didn’t, indicating that abnormal collagen deposition could be contributed to by S100A4.