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Updated: Feb 11, 2026

Studying Triple Negative Breast Cancer Using Orthotopic Breast Cancer Model
Published on: March 20, 2020
miR‑30a inhibits epithelial‑mesenchymal transition and metastasis in triple‑negative breast cancer by targeting ROR1
Xin Wang1, Huisi Qiu2, Ruiming Tang2
1Department of Radiation Oncology, Nan Fang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Abstract:
Triple‑negative breast cancer (TNBC) is a highly aggressive breast cancer subtype that lacks effective targeted therapies. In the present study, we revealed that the expression of miR‑30a was significantly decreased in TNBC, and TNBC patients with low expression of miR‑30a were associated with high histological grade and more lymph node metastasis. Moreover, we found that miR‑30a suppressed TNBC cell epithelial‑mesenchymal transition (EMT), as demonstrated by the overexpression of miR‑30a which increased the expression of epithelial marker E‑cadherin but decreased the expression of mesenchymal markers N‑cadherin and vimentin. Furthermore, we demonstrated that overexpression of miR‑30a significantly suppressed TNBC cell invasion and migration, as well as inhibited tumor growth and metastasis in vivo. More importantly, RTK‑like orphan receptor 1 (ROR1) was predicted as the direct target of miR‑30a, which was subsequently confirmed by luciferase assays. Forced expression of miR‑30a in TNBC cells decreased ROR1 expression, whereas the overexpression of ROR1 reversed the suppressive effects of miR‑30a in TNBC cell migration and invasion. Collectively, this study indicated that miR‑30a functions as a tumor‑metastasis suppressor miRNA in TNBC by directly targeting ROR1 and that miR‑30a may serve as a novel therapeutic target for TNBC.
Insights
MicroRNA-30a (miR-30a) is decreased in triple-negative breast cancer (TNBC), suppressing its growth and metastasis. Targeting miR-30a offers a potential therapeutic strategy for aggressive TNBC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapies.
- MicroRNA-30a (miR-30a) expression is significantly reduced in TNBC.
- Low miR-30a correlates with high histological grade and lymph node metastasis in TNBC patients.
Purpose of the Study:
- To investigate the role of miR-30a in TNBC progression and metastasis.
- To identify the molecular mechanisms underlying miR-30a's function in TNBC.
- To evaluate miR-30a as a potential therapeutic target for TNBC.
Main Methods:
- Quantitative analysis of miR-30a expression in TNBC tissues.
- In vitro studies assessing the effects of miR-30a on epithelial-mesenchymal transition (EMT), invasion, and migration.
- In vivo studies evaluating tumor growth and metastasis inhibition.
- Luciferase assays to confirm the direct targeting of ROR1 by miR-30a.
Main Results:
- miR-30a suppresses TNBC cell EMT by increasing E-cadherin and decreasing N-cadherin and vimentin.
- Overexpression of miR-30a inhibits TNBC cell invasion, migration, tumor growth, and metastasis in vivo.
- RTK-like orphan receptor 1 (ROR1) is identified as a direct target of miR-30a.
- ROR1 overexpression reverses the inhibitory effects of miR-30a on TNBC cell migration and invasion.
Conclusions:
- miR-30a acts as a tumor-metastasis suppressor miRNA in TNBC by directly targeting ROR1.
- Restoring miR-30a levels could be a novel therapeutic strategy for TNBC.
- miR-30a represents a promising therapeutic target for aggressive TNBC.
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