ArticleInternational journal of biological sciences2020
Mifepristone Derivative FZU-00,003 Suppresses Triple-negative Breast Cancer Cell Growth partially via miR-153-KLF5 axis.
Article in International journal of biological sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- LncRNA SNHG15 acts as a ceRNA to promote breast cancer progression through the miR-153-3p/KLF5 signal axis.Journal of Cancer · 2025Article
- Targeting Breast Cancer Stem Cells.International journal of biological sciences · 2023Review
- Research on the effect of interfering with miRNA-155 on triple-negative breast cancer cells.Genes & genomics · 2022Article
- Review
- The role of miR-153 and related upstream/downstream pathways in cancers: from a potential biomarker to treatment of tumor resistance and a therapeutic target.Medical oncology (Northwood, London, England) · 2022Review
- STAMBPL1 promotes breast cancer cell resistance to cisplatin partially by stabilizing MKP-1 expression.Oncogene · 2022Article
- Krüppel-like factor (KLF)5: An emerging foe of cardiovascular health.Journal of molecular and cellular cardiology · 2022Review
- A comprehensive review on miR-153: Mechanistic and controversial roles of miR-153 in tumorigenicity of cancer cells.Frontiers in oncology · 2022Review
- Histone Deacetylase Inhibitors (HDACi) Promote KLF5 Ubiquitination and Degradation in Basal-like Breast Cancer.International journal of biological sciences · 2022Article
- Fasting-mimicking diet blocks triple-negative breast cancer and cancer stem cell escape.Cell metabolism · 2021Article
- The roles and regulation of the KLF5 transcription factor in cancers.Cancer science · 2021Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer (TNBC) is one of the most malignant breast cancers lacking targeted therapeutics currently. We recently reported that mifepristone (MIF), a drug regularly used for abortion, suppresses TNBC cell growth by inhibiting KLF5 expression via inducing miR-153. However, its anticancer efficacy is only modest at high dose. In order to enhance the anticancer activities, a focused compound library containing 17 compounds by altering the sensitive metabolic region of mifepristone has been designed and synthesized. We first tested the cell growth inhibitory effects of these compounds in TNBC cell lines. Among them, FZU-00,003 displayed the most potent efficiency. FZU-00,003 suppresses TNBC cell growth, cell cycle progression and induces apoptosis more effectively than MIF does. Consistently, FZU-00,003 induces miR-153 expression and suppressed KLF5 expression at much lower dosages than MIF does. Furthermore, FZU-00,003 inhibits tumor growth more potently than MIF does. Taken together, the MIF derivative, FZU-00,003 may serve as a better therapeutic compound for TNBC than MIF.
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