Meanwhile, CCR7 functioned as a positive upstream factor of the AKT pathway contributing to the expression of GATA2, promoting trophoblast migration, and invasion via MMP2.
Finally, functional assays were performed and showed that knockdown UBE2Z using small interfering RNA (siRNA) could significantly restrain tumor cell proliferation and suppress cell migration and cell invasion through repressing the expression of MMP2 and MMP9.
Additionally, in vitro assays including epithelial-mesenchymal transition (EMT), metalloproteinase-2 (MMP-2) activity, scratch wound healing, transwell invasion and soft agar colony formation were used to evaluate the effects of 20-HETE agonists/antagonists or GPR75 gene silencing on the aggressive features of PC-3 cells.
Furthermore, Dulcitol surpressed the migration and invasion of HepG2 cells through decreasing the levels of MMP-2, uPA and MMP-9 and increasing E-cadherin associated with tumor invasion.
Mechanistically, c-Myc bound to the BMAL1 promoter and induced BMAL1 transcription, both of which further activated matrix metalloproteinase 2/9 (MMP2/9) and facilitated migration and invasion in HTR-8/SVneo cells.
Urokinase-type plasminogen activator (uPA) has been shown to activate matrix metalloproteinase-2 (MMP-2) that leads to the migration and invasion of breast cancer cells.
Therefore, our findings suggest that MIF may promote the invasion and metastasis of OSCC through the activation of MMP-2 and MMP-9 and prompt further investigation into the therapeutic value of MIF for OSCC treatment.
The silencing of LRP11 in SiHa and CaSki cell lines inhibited cell proliferation, reduced migration and invasion and suppressed cell growth in nude mice, which possibly related to cell cycle protein regulation of CDK 2/4, cyclin D1/E1, MMP-2/9, and VEGF.
Invasion/migration, proteins involved in epithelial-to-mesenchymal transition (EMT), and expression of MMP-2 and HIF-1α were quantified in the CSC subpopulations of two head-and-neck squamous cell carcinoma (HNSCC) cell lines irradiated with X-rays or C-ions.
We show here that ectopic expression of the BIR domains of XIAP specifically resulted in MMP2 activation and cell invasion in XIAP-deleted BC cells, while Src was further defined as an XIAP downstream negative regulator for MMP2 activation and BC cell invasion.
Subsequently, the expression of invasion- and migration-related factors (MMP-2 and MMP-9) and the AKT signaling pathway-related factors (AKT, p-AKT and PI3K-p85) was detected.
Let-7 silencing promoted the proliferation, migration, invasion of HTR8/SVneo cells and the expression levels of MMP-2 and MMP-9, however, it inhibited TIMP-1 and TIMP-2 expression levels, while overexpression of let-7 produced the opposite results.
In parallel, overexpression of RBM6 inhibited invasion and promoted apoptosis of TU212 and Hep-2 cells, as evidenced by downregulation of MMP-2 and MMP-9 protein expression and upregulation of cleaved caspase-3 protein expression.
By using human synoviocyte MH7A cells, TPL was proven to significantly impede migration and invasion of MH7A cells, and also inhibited MMP-2 and MMP-9 expression.
In conclusion, the present study demonstrated that CXCL1 is highly expressed in ER‑negative BC, and stimulates BC cell migration and invasion via the ERK/MMP2/9 pathway.
Moreover, DIE significantly attenuated OSCC cells' motility, migration, and invasion by reducing the MMP-2 protein expression and MMP-2 activity in a dose-dependent manner.
In this study, we provided evidence that 17β-estradiol (E2) could significantly promote endometrial cancer cells viability, migration and invasion through activation of IL-6 pathway, which involved in its downstream pathway and target genes (p-Stat3, Bcl-2, Mcl-1, CyclinD1 and MMP2).
Furthermore, MnTE-2-PyP effectively suppressed TGF-<i>β</i>-mediated cell migration and invasion and the expression of matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 9 (MMP-9) in colorectal cells.
In the rescue experiment, knockdown of HOXD10, accompanied by higher expression of MMP-2/9, could significantly eliminate the inhibitory effects of miR-92b-3p silencing on cell proliferation, migration, and invasion.
Simultaneously, CNMs prepared the cells for migration and invasion by modulating MMP2 and TIMP2 gene expression as well as cytoskeleton reorganization.
In culture, silencing HAT-L4 expression in AML-derived THP-1 cells by short hairpin RNAs inhibited matrix metalloproteinase-2 activation and Matrigel invasion.