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https://www.selleckchem.com/products/wortmannin.html Moreover, inhibition of RRM2 dampened the activation of phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signaling by decreasing phosphorylated-AKT and downstream matrix metalloproteinases-2 expression. Intriguingly, reactivation of the PI3K/AKT pathway with its agonist insulin-like growth factor-1 reversed the adverse effects of RRM2 suppression on cancer cell invasion, migration and VEGF expression. Together, these findings suggest that RRM2 may act as a pro-metastatic factor to facilitate breast cancer metastasis by evoking cell invasion, migration and VEGF expression through the PI3K/AKT signaling pathway. This study may provide an attractive target for metastatic intervention in breast cancer. Copyright © 2020, Spandidos Publications.The present retrospective study aimed to investigate the expression of semaphorin-4C (Sema4C) in epithelial ovarian cancer (EOC), and to determine the association between Sema4C expression and patient clinicopathological characteristics. Sema4C mRNA expression was detected by reverse transcription-quantitative polymerase chain reaction in the tissues of 74 cases of EOC, 20 cases of ovarian epithelial benign tumor, 20 cases of ovarian borderline epithelial tumor and 15 cases of normal ovarian tissue. Immunohistochemistry was used to detect the expression and localization of Sema4C. The association between Sema4C expression level and patients clinicopathological characteristics was determined by χ2 test. The results demonstrated that Sema4C expression level in ovarian epithelial carcinoma tissues was significantly higher compared with that in benign tumors, borderline epithelial tumors and normal ovarian tissues (P less then 0.05). In addition, Sema4C expression in ovarian cancer tissues was significantly associated with the clinical and pathological stages of tumors (P less then 0.05). In conclusion, the present study demonstrated that Sema4C expression was upregulated

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