Targeting TIMM23 to overcome osteosarcoma chemoresistance

Zhiwei Tao1, Pingan Zou2, Zhengxu Yang2

  • 1Bone and Soft Tissue Sarcoma Department, Jiangxi Cancer Hospital, Nanchang, PR China. Tzw2003jx@163.com.

Cell Death & Disease
|November 24, 2025
PubMed

Insights

TIMM23 promotes M2 macrophage polarization via mitophagy, leading to increased osteosarcoma (OS) chemoresistance and tumor growth by upregulating the TIMP2-PARGP1 fusion gene.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Osteosarcoma (OS) chemoresistance is a major therapeutic challenge.
  • Macrophage polarization plays a critical role in tumor microenvironment and treatment response.

Purpose of the Study:

  • Investigate the role of TIMM23 in M2 macrophage polarization and mitophagy.
  • Elucidate the mechanism by which TIMM23 influences OS chemoresistance via the TIMP2-PARGP1 fusion gene.

Main Methods:

  • Single-cell and bulk RNA sequencing, WGCNA, STAR-Fusion, FISH.
  • CRISPR/Cas9 gene editing and lentiviral systems for TIMP2 modulation.
  • Flow cytometry, confocal and transmission electron microscopy, co-culture models, in vitro and in vivo assays.

Main Results:

  • TIMP2 was identified as a key gene in macrophage polarization.
  • TIMP2 promotes M2 polarization through mitophagy.
  • TIMP2-induced M2 polarization upregulates TIMP2-PARGP1 fusion gene expression in OS cells, enhancing proliferation, migration, invasion, and chemoresistance.

Conclusions:

  • TIMP2 enhances OS chemoresistance and progression by promoting M2 macrophage polarization via mitophagy.
  • TIMP2-PARGP1 fusion gene upregulation contributes to OS malignancy and therapeutic failure.