miR-203 Functions as a Tumor Suppressor by Inhibiting Epithelial to Mesenchymal Transition in Ovarian Cancer
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Updated: Mar 26, 2026

Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
Guannan Zhao1, Yuqi Guo2, Zixuan Chen3
1Department 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.
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.
Insights
MicroRNA-203 (miR-203) acts as a tumor suppressor in ovarian cancer by downregulating Snai2. Its overexpression inhibits cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition, leading to reduced tumor growth.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Ovarian cancer is a leading cause of death in women, often due to metastasis and recurrence.
- MicroRNAs (miRNAs) are key regulators of gene expression, acting as either tumor suppressors or oncogenes.
- The specific role of miR-203 in ovarian cancer progression requires further investigation.
Purpose of the Study:
- To investigate the role of miR-203 in ovarian cancer.
- To determine the effect of miR-203 on ovarian cancer cell behavior and tumor growth.
Main Methods:
- miR-203 was overexpressed in ovarian cancer cell lines (SKOV3, OVCAR3) using lentiviral vectors.
- Cell proliferation, migration, and invasion were assessed using MTT, transwell, and Matrigel assays.
- Tumor growth was evaluated in a xenograft mouse model.
Main Results:
- miR-203 was downregulated, and its target Snai2 upregulated in ovarian tumors.
- High miR-203 expression correlated with better patient survival.
- miR-203 overexpression suppressed ovarian cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT).
- Silencing Snai2 mimicked miR-203's inhibitory effects on EMT and invasion.
- Overexpression of miR-203 significantly reduced tumor growth in vivo.
Conclusions:
- miR-203 functions as a tumor suppressor in ovarian cancer.
- miR-203 exerts its tumor-suppressive effects by downregulating Snai2.
- Targeting miR-203 or its pathway may offer therapeutic strategies for ovarian cancer.
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