Moreover, SERPINA3 siRNA could not only reduce live metastasis of mice, but also down-regulate the expression of Mmp-2 and Mmp-9 in liver metastasis tissues.
Moreover, these cells exhibited high metastasis in mice, and p-p65, MMP-2, and MMP-9 expression levels were elevated in the primary tumor and liver metastases.
Overexpression of miR-29c suppresses pancreatic cancer liver metastasis in a nude mouse orthotopic implantation model. miR-29c expression was associated with metastasis and pancreatic cancer patient survival. miR-29c plays an important role in mediating pancreatic cancer metastasis to the liver by targeting MMP2.
Our experimental results suggest that HCS has some anti-metastasis potential to suppress the growth of liver metastasis by decreasing the expression of MMP-2 and MMP-9 as well as VEGF.
Regression analysis indicated that QYHJ possessed an evident inhibition against the progression of liver metastasis by downregulating the expression of VEGF and Cyr61 rather than MMP-2.
We investigated the differential expression of MMP-2, 7, 9, 11, and 13 and their endogenous inhibitors (TIMP-1, 2, and 3) by quantitative real-time RT-PCR in 25 primary tumors, their corresponding lymph node metastases and/or liver metastases and matched normal mucosa.
These findings explain the efficacy of gelatinase-specific synthetic inhibitors on invasion and growth of tumor cells and attribute distinct functions of MMP-2 and MMP-9 to aspects of liver metastasis.
In hepatocellular carcinoma and liver metastases, in situ hybridization showed that MMP2 and TIMP2 mRNA were expressed by anti-alpha-smooth muscle actin-positive cells at the invasive front.
The levels of TIMP-1, MMP-2 and MMP-9 mRNA were significantly higher in primary colorectal cancers than in their adjacent normal tissues, and those of the mRNAs for all four genes were significantly higher in liver metastases than in normal colorectal tissues.