Genetic silencing of PTX3 in invasive melanoma cells dramatically impaired migration and invasion in vitro and in experimental lung extravasation assay in xenografted mice.
R9-ZnC<sup>S334D</sup> also hindered the expression of chemokines and proteins involved in cancer-related inflammation and invasion including Fractalkine (CX3CL1), SDF-1 (CXCL12), MCP-1 (CCL2), NOV (CCN3), and Pentraxin-3 (PTX3).
The effects of both miR-224 and PTX3 on cell proliferation, migration, and invasion were evaluated with an intervention of miR-224 ectopic expression or depletion and PTX3 silencing.
SPOCD1 positively regulated the expression of Pentraxin 3 (PTX3), whereas overexpression of PTX3 attenuated SPOCD1 knockdown-mediated inhibition of cell proliferation, migration and invasion in glioma cells.
In conclusion, PTX3 plays an important role in glioma cell proliferation and invasion, and may thus serve as a novel potential therapeutic target in the treatment of gliomas.
The identification of PTX3 provided a new insight in the interaction between host and tumor and the RI37 peptide showed a great opportunity to largely reduce the risk of invasion and metastasis of cancer and drug-resistant cancers.