Ting Zhu1, Weina Zhang1, Yumin Zhang2, Enbang Lu3, Huayuan Liu4, Xinyue Liu1, Suwei Yin1, Ping Zhang5. 1. Department of Gynecology, Qingdao Municipal Hospital Affiliated to Qingdao University, Qingdao, 266011, People's Republic of China. 2. Institute of Biology, Heze Institute of Food and Drug Inspection and Testing, Heze, 274000, People's Republic of China. 3. Department of Nephrology, Qingdao Municipal Hospital Affiliated to Qingdao University, Qingdao, 266011, People's Republic of China. 4. Qingdao University Medical College, Qingdao, 266071, People's Republic of China. 5. Department of Gynecology, Qingdao Municipal Hospital Affiliated to Qingdao University, Qingdao, 266011, People's Republic of China. zpskx001@163.com.
Abstract
PURPOSE: This study explored the role of irisin/fibronectin type III domain-containing protein 5 (FNDC5) in epithelial ovarian cancer and investigated its underlying mechanisms. METHODS: Immunohistochemistry was performed to analyze the expression of irisin/FNDC5 in epithelial ovarian cancer and normal ovarian tissues. Cell Counting Kit-8, transwell, and wound-healing assays were performed to examine the effect of irisin on the viability, migration, and invasion of ovarian cancer cells, respectively. Western blotting was used to detect the changes of epithelial-mesenchymal transition (EMT)-related proteins and phosphatidylinositol 3-kinase (PI3K)/Akt pathway proteins. Ovarian cancer cells were treated in vitro with the PI3K agonist (740Y-P) in combination with irisin to explore the mechanism of irisin in ovarian cancer. RESULTS: The expression of irisin/FNDC5 in epithelial ovarian cancer tissue was significantly higher than that in normal ovarian tissues, and the expression in late stage patients with lymph node metastasis was lower than that in early stage patients without metastasis. Irisin inhibited the proliferation, invasion, and migration of epithelial ovarian cancer cells, down-regulated phosphorylated Akt, and inhibited EMT progression. The PI3K agonist, 740Y-P, partially reversed the effects of irisin on the invasion, migration, and EMT of ovarian cancer cells. CONCLUSION: These findings show that irisin/FNDC5 was highly expressed in ovarian cancer tissues, which may regulate the EMT through the PI3K/Akt signaling pathway and inhibit the proliferation, invasion, and migration of epithelial ovarian cancer.
PURPOSE: This study explored the role of irisin/fibronectin type III domain-containing protein 5 (FNDC5) in epithelial ovarian cancer and investigated its underlying mechanisms. METHODS: Immunohistochemistry was performed to analyze the expression of irisin/FNDC5 in epithelial ovarian cancer and normal ovarian tissues. Cell Counting Kit-8, transwell, and wound-healing assays were performed to examine the effect of irisin on the viability, migration, and invasion of ovarian cancer cells, respectively. Western blotting was used to detect the changes of epithelial-mesenchymal transition (EMT)-related proteins and phosphatidylinositol 3-kinase (PI3K)/Akt pathway proteins. Ovarian cancer cells were treated in vitro with the PI3K agonist (740Y-P) in combination with irisin to explore the mechanism of irisin in ovarian cancer. RESULTS: The expression of irisin/FNDC5 in epithelial ovarian cancer tissue was significantly higher than that in normal ovarian tissues, and the expression in late stage patients with lymph node metastasis was lower than that in early stage patients without metastasis. Irisin inhibited the proliferation, invasion, and migration of epithelial ovarian cancer cells, down-regulated phosphorylated Akt, and inhibited EMT progression. The PI3K agonist, 740Y-P, partially reversed the effects of irisin on the invasion, migration, and EMT of ovarian cancer cells. CONCLUSION: These findings show that irisin/FNDC5 was highly expressed in ovarian cancer tissues, which may regulate the EMT through the PI3K/Akt signaling pathway and inhibit the proliferation, invasion, and migration of epithelial ovarian cancer.
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