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Updated: Jun 7, 2025

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
MiR-301b-3p promotes breast cancer development through inhibiting the expression of transforming growth factor-beta
Background:
Breast cancer (BC) is a serious health threat to the patients. The present work explored the mechanism of miR-301b-3p and transforming growth factor-beta receptor 2 (TGFBR2 ) in affecting BC progression.
Methods:
The miR-301b-3p-inhibitor and si-TGFBR2 solution were added to the DEME/F12 medium to culture the BC and normal breast epithelial cell lines to prepare negative control, miR-301b-3p-IN and miR-301b-3p-IN+si-TGFBR2 in the two types of cell lines. The relative expression of target genes and the interference effect were analyzed by quantitative real-time PCR (qRT- PCR). Cell viability was detected applying cell counting kit-8 (CCK-8) assay. Transwell and wound healing assay were conducted to evaluate the invasion and migration of BC cells after miR-301b-3p inhibition. Additionally, cell apoptosis and the expression STAT protein were measured by flow cytometry and Western blot, respectively.
Results:
The qRT-PCR results showed that miR-301b-3p were high-expressed but the level of TGFBR2 was significantly inhibited in BC cells. The miR-301b-3p-inhibitor significantly downregulated the expression of miR-301b-3p and upregulated that of TGFBR2. Meanwhile, inhibition of miR-301b-3p suppressed the cell viability, invasion, and migration of BC cells, which, however, were restored by the inhibition of TGFBR2. MiR-301b-3p conferred anti-apoptosis ability to BC cells, while TGFBR2 promoted apoptosis of BC cells through producing an antagonistic effect with miR-301b-3p. We found that miR-301b-3p played a crucial role in the phosphorylation of STAT1 and STAT3 to promote BC progression.
Conclusion:
The present findings demonstrated that miR-301b-3p played a crucial role in promoting BC cell growth, invasion and migration and anti-apoptosis, and that targeting TGFBR2 could inhibit the tumor-promoting effect of miR-301b-3p.
Insights
MicroRNA miR-301b-3p promotes breast cancer (BC) progression by enhancing cell growth, invasion, migration, and inhibiting apoptosis. Targeting transforming growth factor-beta receptor 2 (TGFBR2) counteracts these tumor-promoting effects.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Breast cancer (BC) remains a significant health concern.
- Understanding the molecular mechanisms driving BC progression is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the role of miR-301b-3p in breast cancer.
- To elucidate the mechanism involving miR-301b-3p and transforming growth factor-beta receptor 2 (TGFBR2) in BC progression.
Main Methods:
- Cell culture of BC and normal breast epithelial cells.
- Quantitative real-time PCR (qRT-PCR) for gene expression analysis.
- Cell counting kit-8 (CCK-8), Transwell, and wound healing assays for cell viability, invasion, and migration.
- Flow cytometry for apoptosis analysis and Western blot for STAT protein expression.
Main Results:
- miR-301b-3p was highly expressed in BC cells, while TGFBR2 was inhibited.
- Inhibition of miR-301b-3p suppressed BC cell viability, invasion, and migration, effects reversed by TGFBR2 inhibition.
- miR-301b-3p promoted anti-apoptosis, whereas TGFBR2 promoted apoptosis in BC cells.
- miR-301b-3p influenced STAT1 and STAT3 phosphorylation, promoting BC progression.
Conclusions:
- miR-301b-3p significantly promotes BC cell growth, invasion, migration, and anti-apoptosis.
- Targeting TGFBR2 can effectively inhibit the tumor-promoting effects of miR-301b-3p in breast cancer.
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