Fistein Suppresses Human Osteosarcoma U-2 OS Cell Migration and InvasionviaAffecting FAK, uPA and NF-ĸB Signaling PathwayIn Vitro
| Autor: | Shu-Fen Peng, Jing Gung Chung, An-Cheng Huang, Chin-Chung Lin, Jr-Kai Chen, Hsin-Chung Liu, Yi-Ping Huang, Fu-Shin Chueh, Kuang Chi Lai |
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| Rok vydání: | 2019 |
| Předmět: |
Pharmacology
Cancer Research RHOA biology Chemistry Cell migration medicine.disease General Biochemistry Genetics and Molecular Biology In vitro 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Cell culture 030220 oncology & carcinogenesis biology.protein Cancer research medicine Cytotoxic T cell Osteosarcoma PI3K/AKT/mTOR pathway Fisetin |
| Zdroj: | In Vivo. 33:801-810 |
| ISSN: | 1791-7549 0258-851X |
| Popis: | Background/aim Evidence has indicated that fisetin induces cytotoxic effects in human cancer cell lines, including the inhibition of cell migration and invasion, however, the exact molecular mechanism of action of fisetin in human osteosarcoma cells remains unclear. Materials and methods The anti-metastatic mechanisms of fisetin in human osteosarcoma U-2 OS cells were investigated in vitro. Results Fisetin reduced the viability of cells at different concentrations (2.5, 5 and 10 μM) as measured by flow cytometric assay. Fisetin suppressed cell mobility, migration and invasion of U-2 OS cells, as shown by wound healing assay and transwell filter chambers, respectively. The gelatin zymography assay showed that fisetin inhibited MMP-2 activity in U-2 OS cells. Results from western blotting indicated that fisetin reduced the levels of pEGFR, SOS-1, GRB2, Ras, PKC, p-ERK1/2, p-JNK, p-p-38, VEGF, FAK, RhoA, PI3K, p-AKT, NF-ĸB, uPA, MMP-7, MMP-9, and MMP-13, but increased GSK3β and E-cadherin in U-2 OS cells after 48 h of treatment. Conclusion Fisetin can be used in the future, as a target for the treatment of metastasis of human osteosarcoma cells. |
| Databáze: | OpenAIRE |
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