Related Experiment Video
Updated: Mar 3, 2026

The Use of Mouse Mammary Tumor Cells in an In Vitro Invasion Assay as a Measure of Oncogenic Cell Behavior
Published on: June 12, 2019
miR-217 inhibits triple-negative breast cancer cell growth, migration, and invasion through targeting KLF5
Wenhui Zhou1,2,3, Fangfang Song3,4, Qiuju Wu3,4
1Third Clinical College, Southern Medical University, Guangdong Province, Guangzhou, China.
Abstract:
Triple negative breast cancer (TNBC) is one of the most aggressive breast cancers without effective targeted therapies. Numerous studies have implied that KLF5 plays an important roles in TNBC. How is KLF5 regulated by microRNAs has not been well studied. Here, we demonstrated that miR-217 down-regulates the expression of KLF5 and KLF5's downstream target gene FGF-BP and Cyclin D1 in TNBC cell lines HCC1806 and HCC1937. Consequently, miR-217 suppresses TNBC cell growth, migration, and invasion. MiR-217 suppresses TNBC, at least partially, through down-regulating the KLF5 expression. These results suggest that the miR-217-KLF5 axis might serve as a potential target for treatment of TNBC.
Insights
MicroRNA-217 (miR-217) suppresses triple-negative breast cancer (TNBC) growth by down-regulating KLF5. This miR-217-KLF5 interaction offers a potential therapeutic target for aggressive TNBC.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targeted therapies.
- KLF5 is implicated in TNBC progression, but its microRNA-mediated regulation is unclear.
Purpose of the Study:
- To investigate the role of microRNA-217 (miR-217) in regulating KLF5 expression in TNBC.
- To explore the functional consequences of miR-217-mediated KLF5 suppression on TNBC cell behavior.
Main Methods:
- Utilized TNBC cell lines (HCC1806, HCC1937).
- Assessed the impact of miR-217 on KLF5, FGF-BP, and Cyclin D1 expression.
- Evaluated miR-217's effects on TNBC cell proliferation, migration, and invasion.
Main Results:
- miR-217 was found to down-regulate KLF5 expression in TNBC cells.
- Suppression of KLF5 by miR-217 led to decreased expression of its downstream targets, FGF-BP and Cyclin D1.
- miR-217 significantly inhibited TNBC cell growth, migration, and invasion.
Conclusions:
- miR-217 suppresses TNBC progression, at least partially, by down-regulating KLF5.
- The miR-217-KLF5 axis represents a promising therapeutic target for triple-negative breast cancer treatment.
Related Concept Videos
MicroRNAs
MicroRNAs
Targeted Cancer Therapies
There are several types of targeted therapies against...

