Related Experiment Video
Updated: Mar 26, 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-655 suppresses epithelial-to-mesenchymal transition by targeting Prrx1 in triple-negative breast cancer
Zhi-Dong Lv1, Bin Kong1, Xiang-Ping Liu2
1Department of Breast Surgery, The Affiliated Hospital of Qingdao University, Qingdao, China.
Abstract:
Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype that lacks effective targeted therapies. The epithelial-to-mesenchymal transition (EMT) is a key contributor in the metastatic process. In this study, we found that miR-655 was down-regulated in TNBC, and its expression levels were associated with molecular-based classification and lymph node metastasis in breast cancer. These findings led us to hypothesize that miR-655 overexpression may inhibit EMT and its associated traits of TNBC. Ectopic expression of miR-655 not only induced the up-regulation of cytokeratin and decreased vimentin expression but also suppressed migration and invasion of mesenchymal-like cancer cells accompanied by a morphological shift towards the epithelial phenotype. In addition, we found that miR-655 was negatively correlated with Prrx1 in cell lines and clinical samples. Overexpression of miR-655 significantly suppressed Prrx1, as demonstrated by Prrx1 3'-untranslated region luciferase report assay. Our study demonstrated that miR-655 inhibits the acquisition of the EMT phenotype in TNBC by down-regulating Prrx1, thereby inhibiting cell migration and invasion during cancer progression.
Insights
MicroRNA-655 (miR-655) inhibits triple-negative breast cancer (TNBC) progression by suppressing epithelial-to-mesenchymal transition (EMT). Overexpressing miR-655 reduces cancer cell migration and invasion, offering a potential therapeutic strategy for TNBC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapies.
- Epithelial-to-mesenchymal transition (EMT) is crucial for cancer metastasis.
- miR-655 is downregulated in TNBC and linked to metastasis.
Purpose of the Study:
- To investigate the role of miR-655 in TNBC.
- To determine if miR-655 overexpression can inhibit EMT and metastasis in TNBC.
Main Methods:
- Assessed miR-655 expression in TNBC cell lines and clinical samples.
- Ectopically expressed miR-655 in TNBC cells.
- Evaluated changes in EMT markers (cytokeratin, vimentin).
- Assayed cell migration, invasion, and morphology.
- Investigated the miR-655/Prrx1 interaction using luciferase assays.
Main Results:
- miR-655 expression is reduced in TNBC and correlates with metastasis.
- miR-655 overexpression reversed EMT phenotypes, suppressing migration and invasion.
- miR-655 directly targets and downregulates Prrx1 expression.
- miR-655 inhibits EMT by downregulating Prrx1.
Conclusions:
- miR-655 acts as a tumor suppressor in TNBC.
- miR-655 inhibits TNBC progression by targeting Prrx1 and suppressing EMT.
- miR-655 represents a potential therapeutic target for TNBC treatment.
Related Concept Videos
MicroRNAs
MicroRNAs
Mitogens and the Cell Cycle
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...

