Xue Guan1, Shuo Chen1, Yao Liu1, Li-Li Wang1, Yang Zhao2, Zhi-Hong Zong3. 1. Department of Gynecology, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China. 2. Department of Gynecology, The First Affiliated Hospital of China Medical University, Shenyang, 110001, China. Electronic address: yida.zhaoyang@163.com. 3. Department of Biochemistry and Molecular Biology, College of Basic Medicine, China Medical University, Shenyang, 100013, China. Electronic address: zongzhi_999@163.com.
Abstract
BACKGROUND: Abnormal expression of the PUM1 gene (pumilio RNA binding family member 1) is closely related to chromosomal mutations and carcinogenesis. However, there is no report about expression or function of PUM1 in ovarian cancer. The present study explored the role of PUM1 in the development and progression of ovarian cancer. METHODS: Immunohistochemistry was used to detect the expression of PUM1 in normal ovarian tissues and ovarian cancer tissues. The PUM1 gene was silenced using small interfering RNAs in ovarian cancer cell line A2780. MTT, plate colony formation and EdU (5-ethynyl-2'-deoxyuridine) assays were used to detect cell growth, and cell apoptosis was detected by flow cytometry. Wound-healing and Transwell assays were performed to determine cell migration and invasion. Western blotting was used to detect the levels of cancer-related proteins. RESULTS: Immunohistochemistry showed that the level of PUM1 in ovarian cancer tissues was higher than that in normal tissues. The cell proliferation, migration, and invasion ability decreased significantly, while cell apoptosis increased after silencing the PUM1 gene. Moreover, western blotting showed that downregulation of PUM1 decreased the levels of STAT3, BCL2, MMP2, and VEGFA. CONCLUSIONS: Thus, PUM1 promotes the development and progression of ovarian cancer, which may occur via the above-mentioned molecules.
BACKGROUND: Abnormal expression of the PUM1 gene (pumilio RNA binding family member 1) is closely related to chromosomal mutations and carcinogenesis. However, there is no report about expression or function of PUM1 in ovarian cancer. The present study explored the role of PUM1 in the development and progression of ovarian cancer. METHODS: Immunohistochemistry was used to detect the expression of PUM1 in normal ovarian tissues and ovarian cancer tissues. The PUM1 gene was silenced using small interfering RNAs in ovarian cancer cell line A2780. MTT, plate colony formation and EdU (5-ethynyl-2'-deoxyuridine) assays were used to detect cell growth, and cell apoptosis was detected by flow cytometry. Wound-healing and Transwell assays were performed to determine cell migration and invasion. Western blotting was used to detect the levels of cancer-related proteins. RESULTS: Immunohistochemistry showed that the level of PUM1 in ovarian cancer tissues was higher than that in normal tissues. The cell proliferation, migration, and invasion ability decreased significantly, while cell apoptosis increased after silencing the PUM1 gene. Moreover, western blotting showed that downregulation of PUM1 decreased the levels of STAT3, BCL2, MMP2, and VEGFA. CONCLUSIONS: Thus, PUM1 promotes the development and progression of ovarian cancer, which may occur via the above-mentioned molecules.