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Updated: Mar 8, 2026
Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
miR-503-3p promotes epithelial-mesenchymal transition in breast cancer by directly targeting SMAD2 and E-cadherin
Zitong Zhao1, Xinyi Fan1, Lanfang Jiang1
1State Key Laboratory of Molecular Oncology, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.
Abstract:
Although progress in clinical and basic research has significantly increased our understanding of breast cancer, little is known about the molecular mechanism underlying breast cancer metastasis. Identification of effective therapeutic targets to prevent breast cancer metastasis is urgently needed. The function of miR-503-3p has been investigated in other cancers, but its role in breast cancer remains undefined. Here, we found that miR-503-3p was overexpressed in breast cancer tissue and plasma compared with adjacent normal breast tissue and with plasma from healthy individuals. Moreover, we identified miR-503-3p to be an oncogene of breast cancer cell proliferation, migration and invasion. Upregulation of miR-503-3p in breast cancer cells inhibited expression of epithelial-mesenchymal transition (EMT)-related protein SMAD2 and the epithelial marker protein E-cadherin by directly binding to their mRNA 3' untranslated region, whereas increased expression of mesenchymal marker proteins, including vimentin and N-cadherin. Taken together, our findings support a critical role for miR-503-3p in induction of breast cancer EMT and suggest that plasma miR-503-3p may be a useful diagnostic biomarker for breast cancer.
Insights
MicroRNA miR-503-3p promotes breast cancer growth and metastasis by inhibiting epithelial markers. Plasma miR-503-3p may serve as a diagnostic biomarker for breast cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Breast cancer metastasis lacks defined molecular mechanisms, necessitating new therapeutic targets.
- The role of microRNA miR-503-3p in breast cancer progression is currently unknown.
Purpose of the Study:
- To investigate the function and clinical significance of miR-503-3p in breast cancer.
- To explore miR-503-3p as a potential diagnostic biomarker for breast cancer.
Main Methods:
- Quantitative analysis of miR-503-3p expression in breast cancer tissues and plasma.
- In vitro assays to assess the impact of miR-503-3p on cancer cell proliferation, migration, and invasion.
- Analysis of epithelial-mesenchymal transition (EMT) markers (SMAD2, E-cadherin, vimentin, N-cadherin) following miR-503-3p modulation.
- Luciferase reporter assays to confirm direct binding of miR-503-3p to target mRNAs.
Main Results:
- miR-503-3p was significantly overexpressed in breast cancer tissues and plasma compared to controls.
- Upregulation of miR-503-3p enhanced breast cancer cell proliferation, migration, and invasion.
- miR-503-3p directly targeted SMAD2 and E-cadherin, suppressing epithelial markers and promoting mesenchymal markers (vimentin, N-cadherin), indicating EMT induction.
Conclusions:
- miR-503-3p plays a critical role in inducing epithelial-mesenchymal transition (EMT) in breast cancer.
- Plasma miR-503-3p shows potential as a non-invasive diagnostic biomarker for breast cancer detection.
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