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Protein and Signaling Pathway Responses to rhIL-6 Intervention Before Lobaplatin Treatment in Osteosarcoma Cells

Huan Wang1, Bin Li1, Kang Yan1

  • 1Orthopedic Oncology Institute, Department of Orthopedic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, China.

Frontiers in Oncology
|April 1, 2021
PubMed

Insights

Interleukin-6 (IL-6) reduces osteosarcoma cell sensitivity to lobaplatin, a platinum-based chemotherapy. This study identifies FUBP1 as a key protein driving this resistance, suggesting it as a therapeutic target to improve lobaplatin efficacy.

Area of Science:

  • Oncology
  • Proteomics
  • Molecular Biology

Background:

  • Lobaplatin is a platinum-based chemotherapy agent used for osteosarcoma treatment.
  • Acquired drug resistance, particularly to lobaplatin, is a major challenge in osteosarcoma therapy.
  • Exogenous interleukin-6 (IL-6) has been observed to decrease osteosarcoma cell sensitivity to lobaplatin.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying IL-6-induced lobaplatin resistance in osteosarcoma cells.
  • To identify key proteins involved in the modulation of lobaplatin sensitivity by IL-6.
  • To evaluate the therapeutic potential of targeting identified proteins for overcoming lobaplatin resistance.

Main Methods:

  • Quantitative proteomic analysis using tandem mass tag (TMT) labeling and liquid chromatography-tandem mass spectrometry (LC-MS/MS) on SaOS-2 cells.
  • Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses.
  • Protein-protein interaction (PPI) network analysis, followed by parallel reaction monitoring (PRM) for validation of 31 differentially expressed proteins.

Main Results:

  • A total of 1,313 differentially expressed proteins were identified between treatment groups.
  • Ras GTPase-activating protein-binding protein 1 (G3BP1), fragile X mental retardation syndrome-related protein 1 (hFXR1p), and far upstream element-binding protein 1 (FUBP1) were significantly differentially expressed and validated.
  • High expression of G3BP1, hFXR1p, and FUBP1 was observed in platinum-resistant osteosarcoma patient specimens, correlating with reduced lobaplatin sensitivity.

Conclusions:

  • Interleukin-6 (IL-6) treatment induces lobaplatin resistance in osteosarcoma cells, mediated by significant proteomic alterations.
  • Far upstream element-binding protein 1 (FUBP1) plays a critical role in lobaplatin drug susceptibility in osteosarcoma.
  • Targeting FUBP1, potentially through siRNA knockdown, represents a promising therapeutic strategy to enhance lobaplatin efficacy in resistant osteosarcoma.
Keywords:
FUBP1liquid chromatography-tandem mass spectrometrylobaplatinosteosarcomaprotein–protein interactionrhIL-6 intervention

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