APE1 regulated invasion via upregulation of matrix metalloproteinase 14 (MMP-14), which subsequently activated MMP-2, leading to degradation of the extracellular matrix in a redox-dependent manner.
Inhibitor treatment of metalloproteinases, as well as short hairpin RNA-mediated knockdown of Mmp14 strongly impacted TIC characteristics, including tumor initiation, cell growth, migration, and invasion, especially in starved environments.
Furthermore, the results indicated that miR‑584‑5p inhibited the expression of MMP‑14 at the protein and mRNA levels. miR‑584‑5p also inhibited the expression of MMP‑4 and Slug, which are involved in tumor invasion and metastasis.
Strikingly in this study, ampelopsin E was able to halt migration, transmigration and invasion in MDA-MB-231 cells by reducing formation of invadopodia and its degradation capability through significant reduction (<i>p</i> < 0.05) in expression levels of PDGF, MMP2, MMP9 and MMP14.
NOX5 increases intracellular reactive oxygen species (ROS) that, in turn, activate a HIF1/MMP14 pathway, which is responsible for the increased tumor cell invasion.
Cell proliferation, migration, invasion and the expression of matrix metalloproteinase 2 (MMP-2) and matrix metalloproteinase 14 (MMP-14) after transfection of miR-34a mimics or HNF4α siRNA into SH-SY5Y cells were detected by MTT assay, Transwell assay and Western blot assay, respectively.
Thus, CCAT1 is a key oncogenic lncRNA associated with cervical cancer and plays a role in promoting cervical cancer cell proliferation and invasion by regulating the miR-181a-5p/MMP14 axis.
MT1-MMP is instrumental in SLFN5-controlled inhibition of cancer cell migration and invasion, as shown by MT1-MMP-knockdown and -overexpression analyses.
Membrane type-1 matrix metalloproteinase (MT1-MMP) plays a crucial role in many physiological and pathological processes, especially in tumor invasion and metastasis.
Matrix metalloproteinase 14 (MMP14), a membrane-associated matrix metalloproteinase, has been shown to influence the invasion and metastasis of several solid tumors.
Mechanically, the overexpression of TUG1 significantly up-regulated the levels of MMP-14, VEGF, p-p38 mitogen-activated protein kinase (p-p38 MAPK) and p-HSP27 (heat shock protein 27), and promoted the proliferation, invasion and EMT of Cc cells.
We hypothesized that quantification of membrane type-1 matrix metalloproteinase (MT1-MMP) levels in primary tumor tissue will provide a precise assessment of tumor regional lymph node invasion and remote organ metastasis.
When MT1-MMP was reintroduced into MKN-45 and SGC-7901 cells in the KIF2A-siRNA group, only invasion inhibition effects on MKN-45 and SGC-7901 cells induced by KIF2A silencing can be reversed.
Membrane type 1 metalloproteinase (MT1-MMP) is an important regulator of cancer invasion, growth and angiogenesis, thus making it an attractive target for cancer imaging and therapy.
Analysis of the proteins involved in the invasion showed that there is a significant reduction in the expressions of Rho guanine nucleotide exchange factor 7 (β-PIX), matrix metalloproteinase-9 (MMP-9), and membrane type 1 matrix metalloproteinase (MT1-MMP) in the presence of BHMC treatment at 12.5 µM.