AI Article Synopsis
- This study investigates the role of a specific factor in the metastasis of ovarian cancer by manipulating its expression levels.
- It was found that knocking down this factor suppressed epithelial-mesenchymal transition (EMT) by increasing E-cadherin levels and decreasing Vimentin, while also reducing MMP-2 expression.
- The research suggests that this factor enhances cancer metastasis and EMT by activating the P13K/AKT signaling pathway, indicating its potential as a therapeutic target in ovarian cancer.
Article Abstract
To understand the role of in metastasis of ovarian cancer. By knockdown or overexpression of , we demonstrated the role of in epithelial-mesenchymal transition (EMT). We demonstrated that stable knockdown of suppressed EMT along with the upregulation of E-cadherin and the downregulation of Vimentin. In addition, knockdown decreases matrix metalloproteinase-2 (MMP-2) expression in in vitro cell model and in in vivo nude mice xenografts. The correlation of and MMP-2 expression in the clinical sample confirmed that was tightly correlated with the development of tumor. More importantly, the EMT phenotype and cell invasion induced by overexpressing can be reversed by the siMMP-2 and P13K/AKT signaling inhibitor. contributed to ovarian cancer metastasis and EMT as a positive regulator by activating AKT signaling pathway and inducing MMP-2 expression.
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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6497977 | PMC |
| http://dx.doi.org/10.2147/CMAR.S192950 | DOI Listing |
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