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Updated: Jun 4, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Inhibition of microRNA-660-5p decreases breast cancer progression through direct targeting of TMEM41B
Valeria Villarreal-García1, José Roberto Estupiñan-Jiménez1, Vianey Gonzalez-Villasana2
1Facultad de Ciencias Biológicas, Departamento de Biología Celular y Genética, Universidad Autónoma de Nuevo León, San Nicolás de los Garza, Nuevo León, México.
Background:
Breast cancer is the most prevalent cancer among women worldwide. Most breast cancer-related deaths result from metastasis and drug resistance. Novel therapies are imperative for targeting metastatic and drug-resistant breast cancer cells. Accumulating evidence suggests that dysregulated microRNAs (miRNAs) promote breast cancer progression, metastasis, and drug resistance. Compared with healthy breast tissue, miR-660-5p is notably overexpressed in breast cancer tumor tissues. However, the downstream effectors of miR-660-5p in breast cancer cells have not been fully elucidated. Our aim was to investigate the role of miR-660-5p in breast cancer cell proliferation, migration, invasion, and angiogenesis and to identify its potential targets.
Results:
Our findings revealed significant upregulation of miR-660-5p in MDA-MB-231 and MCF-7 cells compared with MCF-10 A cells. Furthermore, inhibiting miR-660-5p led to notable decreases in the proliferation, migration, and invasion of breast cancer cells, as well as angiogenesis, in HUVEC cells. Through bioinformatics analysis, we identified 15 potential targets of miR-660-5p. We validated TMEM41B as a direct target of miR-660-5p via Western blot and dual-luciferase reporter assays.
Conclusions:
Our study highlights the upregulation and involvement of miR-660-5p in breast cancer cell proliferation, migration, invasion, and angiogenesis. Additionally, we identified TMEM41B as a direct target of miR-660-5p in breast cancer cells.
Insights
MicroRNA-660-5p (miR-660-5p) is upregulated in breast cancer, promoting cell proliferation, migration, invasion, and angiogenesis. Inhibiting miR-660-5p and targeting its effector TMEM41B may offer novel therapeutic strategies.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Breast cancer is a leading cause of cancer death in women, often driven by metastasis and drug resistance.
- Dysregulated microRNAs (miRNAs) are implicated in breast cancer progression, metastasis, and drug resistance.
- miR-660-5p is overexpressed in breast tumors, but its downstream targets and functions remain unclear.
Purpose of the Study:
- To investigate the role of miR-660-5p in breast cancer cell proliferation, migration, invasion, and angiogenesis.
- To identify downstream targets of miR-660-5p in breast cancer cells.
Main Methods:
- Quantitative real-time PCR to measure miR-660-5p expression.
- Functional assays (proliferation, migration, invasion) in breast cancer cell lines.
- Angiogenesis assays using HUVEC cells.
- Bioinformatics analysis to predict miRNA targets.
- Western blot and dual-luciferase reporter assays for target validation.
Main Results:
- miR-660-5p was significantly upregulated in breast cancer cell lines (MDA-MB-231, MCF-7) compared to normal cells (MCF-10A).
- Inhibition of miR-660-5p reduced breast cancer cell proliferation, migration, invasion, and angiogenesis.
- Bioinformatics identified 15 potential miR-660-5p targets; TMEM41B was validated as a direct target.
Conclusions:
- miR-660-5p is upregulated and contributes to breast cancer progression, including proliferation, migration, invasion, and angiogenesis.
- TMEM41B is a direct downstream target of miR-660-5p in breast cancer.
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