Berberine targets epidermal growth factor receptor signaling to suppress prostate cancer proliferation in vitro
| Autor: | Hong‑Fang Zheng, Yong Wang, Qiao‑Xing Li, Zheng‑Hua Huang, Jiu‑Long Wu, Wei‑Lu Wang, Long‑Fei Zhong |
|---|---|
| Rok vydání: | 2014 |
| Předmět: |
Male
Cancer Research Cell cycle checkpoint Berberine Cell Survival Cell Gene Expression Apoptosis Biology Biochemistry chemistry.chemical_compound Cell Line Tumor LNCaP Genetics medicine Humans Epidermal growth factor receptor Molecular Biology Cell Proliferation Epidermal Growth Factor Cell growth Cell Cycle Prostatic Neoplasms Cell Cycle Checkpoints Prostate-Specific Antigen Cell cycle Coptis chinensis biology.organism_classification Molecular biology ErbB Receptors medicine.anatomical_structure Oncology chemistry Cancer research biology.protein Molecular Medicine Signal Transduction |
| Zdroj: | Molecular Medicine Reports. 11:2125-2128 |
| ISSN: | 1791-3004 1791-2997 |
| Popis: | Berberine is a well‑known component of the Chinese herbal medicine Huanglian (Coptis chinensis), and is capable of inhibiting the proliferation of multiple cancer cell lines. However, information available regarding the effect of berberine on prostate cancer cell growth is limited. In the present study, LnCaP and PC‑3 human prostate cancer cell lines were selected as in vitro models in order to assess the efficacy of berberine as an anticancer agent. A cell proliferation assay demonstrated that berberine inhibited cell growth in a dose‑and time‑dependent manner. Further investigation revealed berberine significantly accumulated inside cells that were in the G1 phase of the cell cycle and enhanced apoptosis. Western blot analysis demonstrated that berberine inhibited the expression of prostate‑specific antigen and the activation of epidermal growth factor receptor (EGFR), and it attenuated EGFR activation following EGF treatment in vitro. In conclusion, the results indicate that berberine inhibits the proliferation of prostate cancer cells through apoptosis and/or cell cycle arrest by inactivation of the EGFR signaling pathway. |
| Databáze: | OpenAIRE |
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