| Autor: |
Low, Kaan, Hills, Frank, Roberts, Helen C., Stordal, Britta |
| Předmět: |
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| Zdroj: |
Advanced Biology; Feb2023, Vol. 7 Issue 2, p1-13, 13p |
| Abstrakt: |
Two human osteosarcoma cell lines (MG‐63 and HOS‐143B) are developed into drug‐resistant models using a short‐term drug exposure and recovery in drug‐free media. Cisplatin, doxorubicin, and methotrexate are used as single agents and in triple combination. The highest level of resistance to cisplatin is observed in MG‐63/CISR8, doxorubicin in HOS‐143B/DOXR8, and methotrexate in HOS‐143B/MTXR8. The MG‐63/TRIR8 and HOS‐143B/TRIR8 triple‐resistance models show lower levels of resistance to combination treatment and are not resistant to the drugs individually. Apoptosis assays suggest that the resistance in MG‐63/TRIR8 isfrom cisplatin and methotrexate and not doxorubicin. In contrast, the resistance in HOS‐143B/TRIR8 is from doxorubicin and methotrexate instead of cisplatin. Upregulation of P‐glycoprotein is seen in all resistant models except those developed with single‐agent methotrexate. However, P‐glycoprotein is not causing resistance in all cell lines as the inhibitor elacridar only reverses the resistance of doxorubicin on MG‐63/DOXR8 and HOS‐143B/TRIR8. The migration of the MG‐63 resistant models is significantly increased, their invasion rate tends to increase, and RT‐PCR shows a switch from epithelial to mesenchymal gene signaling. In contrast, a significant decrease in migration is seen in HOS‐143B resistant models with their invasion rate tending to decrease and a switch from mesenchymal to epithelial gene signaling. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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