Guannan Zhao1, Yuqi Guo2, Zixuan Chen3, Yinan Wang4, Chuanhe Yang3, Andrew Dudas3, Ziyun Du3, Wen Liu4, Yanan Zou5, Erzsebet Szabo6, Sue-Chin Lee6, Michelle Sims7, Weiwang Gu8, Todd Tillmanns9, Lawrence M Pfeffer3, Gabor Tigyi6, Junming Yue3. 1. Department of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, USA; Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA; The Third Affiliated Hospital, Zhengzhou University, China. 2. The Third Affiliated Hospital, Zhengzhou University, China. 3. Department of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, USA; Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA. 4. Department of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, USA; Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA; Southern Medical University, Guangzhou, China. 5. Harbin Medical University, P. R. China. 6. Department of Physiology, University of Tennessee Health Science Center, USA. 7. Department of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, USA. 8. Southern Medical University, Guangzhou, China. 9. West Cancer Center, Memphis, TN, USA.
Abstract
OBJECTIVE: Ovarian cancer is a gynecological malignancy that has a high mortality rate in women due to metastatic progression and recurrence. miRNAs are small, endogenous, noncoding RNAs that function as tumor suppressors or oncogenes in various human cancers by selectively suppressing the expression of target genes. The objective of this study is to investigate the role of miR-203 in ovarian cancer. METHODS: miR-203 was expressed in ovarian cancer SKOV3 and OVCAR3 cells using lentiviral vector and cell proliferation, migration, invasion were examined using MTT, transwell and Matrigel assays, respectively. Tumor growth was examined using Xenograft mouse model. RESULTS: miR-203 expression was downregulated, whereas expression of its target gene Snai2 was upregulated in human ovarian serous carcinoma tissue as compared to normal ovaries. In addition, high miR-203 expression was associated with long-term survival rate of ovarian cancer patients. miR-203 overexpression inhibited cell proliferation, migration, and invasion of SKOV3 and OVCAR3 ovarian cancer cells. Furthermore, miR-203 overexpression inhibited the epithelial to mesenchymal transition (EMT) in ovarian cancer cells. Silencing Snai2 with lentiviral short hairpin (sh) RNA mimics miR-203-mediated inhibition of EMT and tumor cell invasion. Xenografts of miR-203-overexpressing ovarian cancer cells in immunodeficient mice exhibited a significantly reduced tumor growth. CONCLUSION: miR-203 functions as a tumor suppressor by down regulating Snai2 in ovarian cancer.
OBJECTIVE:Ovarian cancer is a gynecological malignancy that has a high mortality rate in women due to metastatic progression and recurrence. miRNAs are small, endogenous, noncoding RNAs that function as tumor suppressors or oncogenes in various humancancers by selectively suppressing the expression of target genes. The objective of this study is to investigate the role of miR-203 in ovarian cancer. METHODS:miR-203 was expressed in ovarian cancerSKOV3 and OVCAR3 cells using lentiviral vector and cell proliferation, migration, invasion were examined using MTT, transwell and Matrigel assays, respectively. Tumor growth was examined using Xenograft mouse model. RESULTS:miR-203 expression was downregulated, whereas expression of its target gene Snai2 was upregulated in humanovarian serous carcinoma tissue as compared to normal ovaries. In addition, high miR-203 expression was associated with long-term survival rate of ovarian cancerpatients. miR-203 overexpression inhibited cell proliferation, migration, and invasion of SKOV3 and OVCAR3 ovarian cancer cells. Furthermore, miR-203 overexpression inhibited the epithelial to mesenchymal transition (EMT) in ovarian cancer cells. Silencing Snai2 with lentiviral short hairpin (sh) RNA mimics miR-203-mediated inhibition of EMT and tumor cell invasion. Xenografts of miR-203-overexpressing ovarian cancer cells in immunodeficientmice exhibited a significantly reduced tumor growth. CONCLUSION:miR-203 functions as a tumor suppressor by down regulating Snai2 in ovarian cancer.
Entities:
Keywords:
Epithelial to mesenchymal transition; Ovarian cancer; miR-203
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