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https://www.selleckchem.com/TGF-beta.html Further, through RT-qPCR tests, the expressions of PTGS2 and SQLE were proven to be significantly upregulated in normal pancreatic duct epithelia cell (HPDE6-C7) compared to pancreatic cancer cells (SW1990 and BxPC-3). MTT, wound-healing and transwell assays revealed that silencing PTGS2 and SQLE could inhibit the proliferation, migration and invasion of pancreatic cancer cells. Besides, western-blot assays showed that blocking PTGS2 and SQLE expressions could suppress the protein expressions of cyclin D1 and N-cadherin, but facilitate that of E-cadherin, which suggested that they were involved in the epithelial to mesenchymal transition (EMT). Collectively, FR risk signature provides an important complement for PAAD prognostic analysis. High FR risk level can adversely affect anti-tumor immune process, but may not serve as a predictive marker of ICIs efficacy. PTGS2 and SQLE are proven to possess cancer-promoting abilities in PAAD. The aim of this study is to determine the therapeutic effects of boric acid cell proliferation, invasion, migration, colony formation, cell cycle and apoptosis mechanisms in ovarian cancer cell line under in vitro conditions. MDAH-2774 ovarian cancer cells were employed. Real-time PCR test was used to investigate changes in genes and proteins of cell cycle and apoptosis and identified miRNAs under the addition of boric acid. The apoptosis rates were calculated by TUNEL assay. Matrigel invasion, colony formation and Wound healing tests were used to determine invasion and migration. Oxidative stress index value was calculated for oxidative stress. Boric acid inhibited cell proliferation, invasion, migration and colony formation, but induces apoptosis and oxidative stress. Also, the expression of miRNA-21, miRNA-200a, miRNA-130a and mi-RNA-224 (which are indicators of poor prognosis of ovarian cancer) decreased significantly. The potential of boric acid as a natural molecule may supports its effecti

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