Bioinformatic analysis and western blotting showed that PSAP mainly played a regulatory role in GBM invasion and EMT-like processes via the TGF-β1/Smad signaling pathway.
UCA1 knockdown ameliorated, whereas miR-124 inhibition exacerbated TGFβ1-induced EMT and invasion in tongue cancer cells through miR-124 downstream jagged 1 (JAG1) and Notch signaling.
The results indicated that TGF-β1 induced spindle-shaped changes, increased migration and invasion, and upregulated or downregulated the relative expression of EMT biomarkers.
Further studies indicated that additional treatment with TGF-β1 could markedly abrogate FMNL1 knockdown-induced suppression of migration and invasion in NSCLC cells.
NEF expression vector was transfected into CSCC cells and the effects on cell migration and invasion as well as TGF-β1 expression were investigated by Transwell migration assay, Transwell invasion assay, and Western blot, respectively.
Treatment with TGF-β1 demonstrated no significant effect on AWPPH expression; however, a TGF-β inhibitor attenuated the effects of AWPPH overexpression on cell migration and invasion.
In HNSCC cell lines, PRRX1 positively promoted the expression of known EMT inducers and cooperated with activated TGF-β1 to contribute to EMT and migration and invasion of HNSCC cells.
The compound also significantly inhibited the phosphorylation of Axl and dose dependently inhibited cell invasion and migration in TGF-β1 induced MDA-MD-231 breast cancer cells.
These results demonstrated that overexpression of SMS1 inhibited TGF‑β1‑induced EMT and the migration and invasion of MDA‑MB‑231 cells, increasing the expression of E‑cadherin while decreasing the expression of vimentin.
MSH6, CXCR4 and TGFB1 formed a triangular MSH6-CXCR4-TGFB1 feedback loop that accelerated gliomagenesis, proliferation (G1 phase), migration and invasion (epithelial-to-mesenchymal transition; EMT), stemness, angiogenesis and antiapoptotic effects by regulating the p-STAT3/Slug and p-Smad2/3/ZEB2 signaling pathways in GBM.
The expression of Pard3 was increased by the inhibition of miR-483, but TGF-β1-induced cell migration and invasion were decreased by miR-483 inhibition.
COX-2 inhibitors and antagonists of PGE<sub>2</sub> and PGD<sub>2</sub> receptors reversed the inhibition of TGF-β1-induced EMT, migration, and invasion by Gas6.