Mechanism dissection revealed that R-2HG could increase circRNA-51217 expression to increase the sponge miRNA-646, which might then lead to increase TGFβ1 expression and thus induce TGFβ1/p-Smad2/3 signaling to increase PCa cell invasion.
ALDH1 expression as detected by immunohistochemical staining was associated with high nodal stage, advanced clinical stage, lymphatic invasion and poor survival (P=0.01, P=0.04, P<0.05 and P<0.01, respectively) and with the expression of TGF-β1 and β-catenin.
Transwell invasion and migration assays showed that MIR4435-2HG and TGF-β1 promoted the invasion and migration of OC cells while TGF-β inhibitor suppressed the invasion and migration of these cells.
Recent research suggests Foxp3(+) CD4(+)CD25(+)-expressing T regulatory (Treg) cells play a role in regulation of the immunopathology of granulomas in experimental toxocaral granulomatous hepatitis and in enhanced expression of TGF-β1, which is an important factor for the local survival and function of Treg observed during T. canis invasion in the mouse small intestine, liver, muscle, and brain.
Wound healing and invasion assay were employed to investigate the role of <i>CCAT1</i> and <i>miR</i>-<i>490</i>-<i>3p</i> in the TGFβ1-induced migration and cell invasion of ovarian cancer cells, respectively.
High glucose promotes tumor invasion and increases metastasis-associated protein expression in human lung epithelial cells by upregulating heme oxygenase-1 via reactive oxygen species or the TGF-β1/PI3K/Akt signaling pathway.
Furthermore, exogenous inhibition of PDE4A or activation of cAMP/PKA/CREB signalling rescued TGF-β1 expression, EMT and invasion in autophagy-deficient hepatocarcinoma cells.
Down-regulation of lncRNA snaR effectively distinguished HPV-negative CSCC patients from healthy controls. lncRNA snaR was further down-regulated in patients with distant recurrence (DR) but not in patients with local-recurrence or without recurrence. lncRNA snaR overexpression decreased TGF-β1 expression in CSCC cells, while exogenous TGF-β1 treatment showed no significant effects on lncRNA snaR expression. lncRNA snaR overexpression inhibited cancer cell migration and invasion, while TGF-β1 treatment attenuated the inhibitory effect of lncRNA snaR overexpression on cancer cell migration and invasion.
The potential roles of TSN on GC cells were examined and it was found that TSN inhibited growth, migration, invasion and TGF‑β1-induced epithelial-mesenchymal transition (EMT) and induced cell cycle arrest and apoptosis in SGC‑7901 cells which were most sensitive to TSN among various GC cell lines.
Matrix metalloproteinase (MMP)-9 plays an important role in tumor invasion and metastasis, and its expression is regulated by various growth factors, including TGF-β1, in different cell types.
Recently, we discovered another mode through which PAR2 may enhance tumorigenesis: crosstalk with transforming growth factor-β (TGF-β) signaling to promote TGF-β1-induced cell migration/invasion and invasion-associated gene expression in ductal pancreatic adenocarcinoma (PDAC) cells.
Our results demonstrated that sauchinone significantly inhibited transforming growth factor-β1 (TGF-β1)-induced migration and invasion in gastric cancer cells.
Markers relevant for bulk cancer cell migration were regulated differently when compared with EMT: Twist expressed in primary tumour, invasion front, and metastasis was not associated with TGFβ1 and canonical Wnt, as Slug, Snail, and Smads were negative and β-Catenin expressed membraneously.
Moreover, transforming growth factor-β1-mediated inhibition of microRNA -196a-3p and activation of neuropilin-2were required for transforming growth factor-β1-induced migration and invasion of breast cancer cells.
Taken together, DKK1 appears to facilitate tumor invasion and migration through TGF- β1 by remodeling the tumor microenvironment and inducing inflammation.
These results indicate that TGF-β1 could promote S. aureus adhesion to and invasion into BMFBs by increasing Collagen I and α-SMA expression and may provide a novel target for controlling bovine mastitis.
We observed reduced EMT in ovarian cancer cells upon co-activation with TGFβ1 and LiCl as shown by the expressions of epithelial/mesenchymal markers and the EMT promoting factor, Snail1, accompanied by decrease in the invasion and migration of the cells compared to individual pathway activation.
Relative overexpression of the TGF-beta1 gene was associated with advanced UICC stage (III/IV vs. I/II; P = 0.009), depth of tumor infiltration (pT3 vs. pT1/2; P < 0.001), nodal involvement (pN1 vs. pN0; P = 0.006), and lymphatic vessel invasion (L1 vs. L0; P = 0.011).