Silencing of STC2 in the CRC Sw480 cells increased the expression of E‑cadherin and decreased the expression of vimentin, MMP‑2 and MMP‑9, compared to those in the normal and empty vector group.
Procollagen-lysine, 2-oxoglutarate 5-dioxygenase 1 (<i>PLOD1</i>) and matrix metalloproteinase 9 (<i>MMP9</i>) were selected to assess the DNA methylation of the WBCs from CRC patients using real-time methylation-specific PCR.
JMJD2D was required for expression of β-catenin in CRC cell lines; ectopic expression of JMJD2D increased the promoter activities of genes regulated by β-catenin (MYC, CCND1, MMP2, and MMP9).
These results indicated that sevoflurane suppressed cell migration and invasion through regulating ERK/MMP-9 pathway via miR-203/Robo1 in CRC cells, indicating important clinical implications for anesthetic agents to prevent metastasis in CRC.
In addition, PEC markedly impaired CRC cell migration and invasion by downregulating the expression of matrix metalloproteinase (MMP-9) and phosphorylated-Stat3<sup>Tyr705</sup>.
We investigate redox state-superoxide (SO) generation rate, activity of complex I in electron transport chain (ETC) of mitochondria and of dinitrosyl iron complexes by electron paramagnetic resonance; activity of matrix metalloproteinase (gelatinase) MMP-2 and MMP-9 by gel zymography of adipose tissues (AT) from 46 patients (64.0 ± 1.6 y.o.) with CRC (II-III stages, pT2-3N0-2M0) in the AT adjacent to tumor (ATAT) and at a distance of 3 cm from the tumor (ATD) to follow the connection of the AT redox state with some of the tumor microenvironment indicators.
This resulted in the increased expression of matrix metalloproteinase 2 (MMP2), matrix metalloproteinase 9 (MMP9) and vascular endothelial growth factor (VEGF), and the subsequent promotion of CRC cell invasion.
The expression of Rap1GAP, matrix metallopeptidase 9 (MMP-9) and E-cadherin in 227 CRC tissues and paired para-carcinoma tissues was detected by immunohistochemistry.
Combination of Stat5 or MMP inhibitors with immunotherapy could help repolarize CRC TINKs and TANKs to anti-tumor antimetastatic ones.-Bruno, A., Bassani, B., D'Urso, D. G., Pitaku, I., Cassinotti, E., Pelosi, G., Boni, L., Dominioni, L., Noonan, D. M., Mortara, L., Albini, A. Angiogenin and the MMP9-TIMP2 axis are up-regulated in proangiogenic, decidual NK-like cells from patients with colorectal cancer.
These results illustrated that low dose colchicine efficiently induced cell death and apoptosis of SW480 cells and the inhibition of MMP-9 mRNA levels was significantly correlated with the amount of cellular colchicine uptake, suggesting that colchicine has a potential value in the treatment of human colorectal cancer.
Herein we describe construction of a nanosensor for matrix metalloproteinase 9 (MMP9), which is associated with tumor progression and metastasis, for detection of colorectal cancer in a mouse model.
Our aim was to assess the activity of MMP-2 and MMP-9 and its relation to the parameters of oxidative stress and membrane damage markers in patients with different TNM (tumour, lymph nodes, metastasis) stages of colorectal carcinoma.
In conclusion, Rab1B and MMP9 are potential prognostic biomarkers and their combination significantly improves predictive power for survival and chemotherapy response in CRC patients.
The present study noticed significantly increased activity of active MMP-2 and MMP-9 in tumor tissues (P<0.01), and significantly decreased levels of pro-form MMP-2 and MMP-9 in tumor tissues (P<0.01), compared with that in adjacent tissues in patients with CRC.
In the present study, it was hypothesized that KiSS-1 gene could repress the metastatic potential of colorectal cancer cells by inhibiting the expression of MMP-9.