Progressive resistance of BTK-143 osteosarcoma cells to Apo2L/TRAIL-induced apoptosis is mediated by acquisition of DcR2/TRAIL-R4 expression: resensitisation with chemotherapy
2003

Resistance of Osteosarcoma Cells to Apo2L/TRAIL and Chemotherapy Resensitization

publication Evidence: moderate

Author Information

Author(s): Bouralexis S, Findlay D M, Atkins G J, Labrinidis A, Hay S, Evdokiou A

Primary Institution: University of Adelaide

Hypothesis

The study investigates how the expression of DcR2/TRAIL-R4 contributes to the resistance of BTK-143 osteosarcoma cells to Apo2L/TRAIL-induced apoptosis and whether chemotherapy can resensitize these cells.

Conclusion

The study found that BTK-143 osteosarcoma cells become resistant to Apo2L/TRAIL due to increased expression of DcR2, but this resistance can be reversed with chemotherapy.

Supporting Evidence

  • BTK-143 cells showed increased DcR2 expression with repeated culture passages.
  • Chemotherapy agents like DOX, CDDP, and ETP resensitized resistant BTK-143 cells to Apo2L/TRAIL-induced apoptosis.
  • Blocking DcR2 restored sensitivity to Apo2L/TRAIL in late-passage BTK-143 cells.

Takeaway

Some cancer cells can become resistant to treatments that usually kill them, but using certain chemotherapy drugs can help make them sensitive again.

Methodology

The study used human osteosarcoma cell lines to assess the effects of Apo2L/TRAIL and various chemotherapeutic agents on cell viability and receptor expression.

Limitations

The study primarily focuses on a single cell line, which may not represent all osteosarcoma cases.

Digital Object Identifier (DOI)

10.1038/sj.bjc.6601021

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