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.
Transforming growth factor-β1 (TGF-β1), chemokine Stromal cell-derived factor-1 (SDF-1) and its endogenous receptor CXCR4 may play important roles during this process.<b>Methods</b>: Co-culture technique was used to explore the effects of MSCs on the proliferation, migration and invasion of colorectal carcinoma (CRC) cells and how they induced MSCs to differentiate into CAFs.
Collectively, TMEM158 was upregulated in PC and promoted PC cell proliferation, migration, and invasion through the activation of TGFβ1 and PI3K/AKT signaling pathways, highlighting its potential as a tumor promoter and a therapeutic target for PC.
The enhancement in invasion and migration of TGF-β1-induced A549 cells was inhibited by Sch B. Sch B also repressed the expression of ZEB1 transcription factor in EMT, by increasing the enrichment of H3K9me3 at the ZEB1 promoter to repress its transcription while the expression of the Twist1 transcription factor was unaffected.
On the other hand, TGF-β1-induced proliferation, migration and invasion were suppressed by function-blocking antibody against integrin αMβ2 in RCC cells.
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.
Taken together, DKK1 appears to facilitate tumor invasion and migration through TGF- β1 by remodeling the tumor microenvironment and inducing inflammation.
Both miR-144-3p overexpression and Src inhibition could obviously inhibit the invasion and adhesion abilities of A549 cells in the presence or absence of the effects of TGF-β1.
MAP 1B-LC1 was identified and validated as one of the proteins interacting with hnRNP K. Knockdown of MAP 1B-LC1 repressed E-cadherin downregulation, vimentin upregulation and actin filament remodeling, decreased cell migration and invasion during TGF-β1-induced EMT in A549 cells. hnRNP K increased microtubule stability via interacting with MAP 1B-LC1 and was associated with acetylated ɑ-tubulin during EMT.
Epigallocatechin gallate (EGCG) suppresses epithelial-Mesenchymal transition (EMT) and invasion in anaplastic thyroid carcinoma cells through blocking of TGF-β1/Smad signaling pathways.
In conclusion, our study proved that 12-LOX/12-HETE-promoted tumor migration and invasion might partly be through TGF-β1-mediated EMT in ESCC, and 12-LOX could be a promising biomarker for predicting prognosis in ESCC patients.
Notably, the suppression experiments of metastatic activities reveal that 10n also displays significant anti-metastasis effects through inhibiting cell migration and invasion in highly metastatic SMMC-7721 cell line, and dose-dependently reverses TGF-β1-induced epithelial-mesenchymal transition (EMT) procedure better than ADM.
Taken together, the results of the present study suggest that miR‑142‑3p may serve an important role in human placental development by suppressing trophoblast cell invasion and migration through disruption of the TGF‑β1/smad3 signaling pathway, suggesting that knockdown of miR‑142‑3p may provide a novel therapy for PE.
Collectively, our study suggests that the downregulation of LOX and LOXL2 leading to reduced trophoblast cell migration and invasion through activation of the TGF-β1/Smad3/collagen pathway is relevant to preeclampsia.