These findings further reveal the possible mechanism and effect of the miR-429/CrkL/MMP-9 regulatory axis in the bone microenvironment in breast cancer bone metastasis.
We observed a significant increase in the level of MMP-9 mRNA expression in breast cancer patients in comparison to their normal breast tissues and to tissues of benign breast disease.
Light microscopy showed a higher concentration of cells with positive cytoplasmic staining for MMP-2 and MMP-9 expression in breast cancer than in fibroadenoma.
Moreover, RT-PCR results showed that RSF EtOAc significantly downregulated MMP-2 and MMP-9 expression, which play an important role in breast cancer metastasis.
Furthermore, we verified that knockdown of lncRNA PANDAR dramatically inhibited cell epithelial-mesenchymal transition (EMT) pathway by downregulating Vimentin, MMP2 and MMP9 expression, but upregulating E-cadherin expression in breast cancer.
Moreover, the levels of MMP-9 were significantly increased in larger tumor size (T3/T4) (p < 0.05) as compared to smaller size (T1/T2), which suggests that MMP-9 plays an important role in the progression of breast cancer.
Arylamine <i>N</i>-Acetyltransferase 1 Regulates Expression of Matrix Metalloproteinase 9 in Breast Cancer Cells: Role of Hypoxia-Inducible Factor 1-<i>α</i>.
We focused on the clinical relevance of ENO1 and MMPs (MMP-2 and MMP-9) overexpression in breast cancer tissues: The association between the higher ENO1, MMP-2 and MMP-9 expression with a worse prognosis suggest that the elevated ENO1 and MMPs expression are promising biomarkers for breast cancer.
As2S2 treatment also inhibited the protein expression of matrix metalloproteinase‑9 (MMP‑9), but increased the intracellular accumulation of ROS in the two breast cancer cell lines, which may assist in alleviating metastasis and attenuating the progression of breast cancer.
Similarly, F3 significantly reduced the expression of MMP-9, MUC1, N-cadherin, Twist, VEGF and vimentin in comparison with the TM (p < 0.01) group CONCLUSIONS: Our findings suggest that F3 exerts anti-metastatic effects independent of its cytotoxic effects, and these are supported by the increased expression of E-cadherin concurrent with downregulation of MMP-9, MUC1, N-cadherin, Twist, VEGF and vimentin expression in breast cancer.
Our studies demonstrate for the first time that the function of MMP2 and MMP9 in breast cancer cell migration, which is mediated by interactions between ERα-36 and STAT3.
This study aim to investigate the association of breast cancer risk and prognostic factors with single nucleotide variants of the <i>BRCA1</i>, <i>BRCA2</i>, <i>DAPK1, MMP9, TOX3</i>, and <i>TP53</i> genes in Jordanian women.
This study confirmed a new mechanism by which BMAL1 up-regulated MMP9 expression to increase breast cancer metastasis, to provide research support for the prevention and treatment of breast cancer.
At the same time, M@BS-QE NPs down-regulated p-Akt and matrix metalloproteinase-9 (MMP-9, which degrades the extracellular matrix to promote invasion and metastasis of tumors) signal axis to suppress breast cancer lung metastasis.
Application of ADAM8 and MMP-9 antibodies reduced transmigration of MB-231 cells suggesting that ADAM8 affects transmigration of breast cancer cells by MMP-9 regulation.
In summary, inhibition of Src kinase suppressed TNBC tumor growth and metastasis, and Src inhibitors such as BJ-2302 may constitute a novel therapeutic tool to treat breast cancer that expresses high levels of CTSS and MMP-9.