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.
Highlights
Breast cancer is still the main cause of female cancer-related death in United States [1]
The expression of Kruppel-like factor 5 (KLF5) is correlated with different hormone status in different breast cancer subtypes [8]
Accumulated evidence suggests that KLF5 is an oncogene in Triplenegative breast cancer (TNBC) [7, 10, 12,13,14,15, 36]
Summary
Breast cancer is still the main cause of female cancer-related death in United States [1]. Triplenegative breast cancer (TNBC), which lacks expression of estrogen receptor α (ERα) and progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2) gene, accounts for approximately 15% of breast cancers [2]. TNBC is more aggressive, has higher rates of relapse and shorter overall survival than other subtypes of breast cancers. The median survival of women with metastatic TNBC is less than 12 months [3]. There are still no effective targeted therapies for TNBC. It’s urgent to identify effective therapeutic targets for TNBC
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