Galangin Inhibits Cholangiocarcinoma Cell Growth and Metastasis through Downregulation of MicroRNA-21 Expression
Autor: | Meiling Zuo, Lijuan Liu, Wencheng Gong, Fangfang Tou, Wenqun Li, Min Zhou, Yin Chen, Yang Zou, Dabin Kuang, Li Jiang, Wei Tong, Rong Li |
---|---|
Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Article Subject Down-Regulation Antineoplastic Agents Apoptosis General Biochemistry Genetics and Molecular Biology Cholangiocarcinoma 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Downregulation and upregulation Cell Movement Cell Line Tumor Tensin PTEN Humans Protein kinase B Cell Proliferation Flavonoids General Immunology and Microbiology biology Kinase Cell growth General Medicine Galangin MicroRNAs 030104 developmental biology chemistry Bile Duct Neoplasms 030220 oncology & carcinogenesis Cancer research biology.protein Medicine Research Article Signal Transduction |
Zdroj: | BioMed Research International BioMed Research International, Vol 2020 (2020) |
ISSN: | 2314-6141 2314-6133 |
Popis: | Galangin, a natural flavonoid product derived from the root of galangal, is emerging as a promising anticancer agent against multiple cancers. Yet, whether it also has antitumor effects on cholangiocarcinoma (CCA) and the underlying mechanism is still unknown. Herein, we demonstrate that galangin exhibits multiple antitumor effects on CCA cells including decreases cell viability; inhibits proliferation, migration, and invasion; and induces apoptosis. Moreover, those phenotypic changes are associated with downregulated microRNA-21 (miR-21) expression. To support, overexpression of miR-21 blocks galangin-mediated antisurvival and metastasis effects on CCA cells. Mechanically, galangin increases the expression of phosphatase and tensin homolog (PTEN), a direct target of miR-21, resulting in decreased phosphorylation of AKT, a protein kinase which plays a critical role in controlling survival and apoptosis. In contrast, overexpression of miR-21 abrogates galangin-regulated PTEN expression and AKT phosphorylation. Taken together, these findings indicate that galangin inhibits CCA cell proliferation and metastasis and induces cell apoptosis through a miR-21-dependent manner, and galangin may provide a novel potential therapeutic adjuvant to treat CCA. |
Databáze: | OpenAIRE |
Externí odkaz: |