Furthermore, inhibition of activated the ASIC2-mediated calcineurin/NFAT1 pathway and target gene transcript expression of MMP-2 and MMP-9 in parallel to reduce, and resulted in the reduced invasion ability by TER treatment.
NFAT1 knockdown reduced GSC viability, invasion, and self-renewal <i>in vitro</i> and inhibited tumorigenesis <i>in vivo</i>, whereas NFAT1 overexpression enhanced the growth and invasion of GSCs.
By combining predictor genes of six downregulated miRNAs and dysregulated genes of the WNT pathway, we inferred that overexpression of CHAP2 may inhibit LUAD cell proliferation and invasion via modulation of NFATC2 or GSK3B (WNT signal pathway) targeted by miR-3614-5p or miR-873-3p.
NFAT1 overexpression significantly strengthened the melanoma-conditioned TAM-mediated promotion of cell migration and invasion in A375 and WM451 cells, whereas NFAT1 knockdown exerted the opposite effects.
Double knockdown of MDM2 and NFAT1 also revealed that the expression of both of these molecules is important for InuA's inhibitory effects on the proliferation and invasion of prostate cancer cells.
Invasion by cancer cells has been associated with NFAT1 (nuclear factor of activated T cells) activation and expression of the COX-2 (cyclooxygenase 2) gene.