KDELR1 regulates chondrosarcoma drug resistance and malignant behavior through Intergrin-Hippo-YAP1 axis

Cell Death Dis. 2024 Dec 23;15(12):928. doi: 10.1038/s41419-024-07264-7.

Abstract

Chondrosarcoma (CS) is the second most common primary bone malignancy, known for its unique transcriptional landscape that renders most CS subtypes resistant to chemotherapy, including neoadjuvant chemotherapy commonly used in osteosarcoma (OS) treatment. Understanding the transcriptional landscape of CS and the mechanisms by which key genes contribute to chemotherapy resistance could be a crucial step in overcoming this challenge. To address this, we developed a single-cell transcriptional map of CS, comparing it with OS and normal cancellous bone. Our analysis revealed a specific increase in KDEL receptor 1 (KDELR1) expression in CS, which was closely associated with CS prognosis, tumor aggressiveness, and drug resistance. KDELR1 plays a key role in regulating membrane protein processing and secretion, as well as contributing to tumor extracellular matrix (ECM) formation and drug resistance. Further investigation using mass spectrometry proteomics and transcriptomics uncovered KDELR1's involvement in modulating the Hippo-YAP pathway activity in CS cells. The KDELR1-Integrin-PLCγ-YAP1 axis emerges as a critical process mediating drug resistance and malignant behavior in CS, offering novel insights and potential therapeutic targets for CS treatment.

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics
  • Adaptor Proteins, Signal Transducing / metabolism
  • Animals
  • Bone Neoplasms* / drug therapy
  • Bone Neoplasms* / genetics
  • Bone Neoplasms* / metabolism
  • Bone Neoplasms* / pathology
  • Cell Line, Tumor
  • Chondrosarcoma* / drug therapy
  • Chondrosarcoma* / genetics
  • Chondrosarcoma* / metabolism
  • Chondrosarcoma* / pathology
  • Drug Resistance, Neoplasm* / genetics
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects
  • Hippo Signaling Pathway
  • Humans
  • Male
  • Mice
  • Osteosarcoma / drug therapy
  • Osteosarcoma / genetics
  • Osteosarcoma / metabolism
  • Osteosarcoma / pathology
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism
  • Receptors, G-Protein-Coupled / genetics
  • Receptors, G-Protein-Coupled / metabolism
  • Signal Transduction / drug effects
  • Transcription Factors / genetics
  • Transcription Factors / metabolism
  • YAP-Signaling Proteins* / metabolism

Substances

  • YAP-Signaling Proteins
  • YAP1 protein, human
  • Adaptor Proteins, Signal Transducing
  • Transcription Factors
  • Receptors, G-Protein-Coupled
  • Protein Serine-Threonine Kinases