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CBX7 regulates chemotherapy-induced senescence-like growth arrest in multiple myeloma via the ERK/STAT3/PIM1 axis

Yangyang Ding1,2,3, Zelin Liu1,2, Ya Liao1,2

  • 1Department of Hematology/Hematological Lab, The Second Affiliated Hospital of Anhui Medical University, No. 678 Furong Road, Hefei, Anhui, 230031, China.

Journal of Translational Medicine
|November 18, 2025
PubMed
Abstract

Insights

Cellular senescence drives multiple myeloma (MM) progression and relapse. Targeting CBX7, a key regulator of senescence, and its ERK/PIM1 pathway may enhance bortezomib chemotherapy efficacy in MM patients.

Area of Science:

  • Oncology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Chemotherapy resistance and relapse in multiple myeloma (MM) are linked to cellular senescence.
  • Bortezomib (BTZ) is a proteasome inhibitor used in MM treatment.
  • Understanding myeloma cell senescence drivers is crucial for improving MM outcomes.

Purpose of the Study:

  • To investigate the key drivers of myeloma cell senescence.
  • To elucidate the role of cellular senescence in MM progression.
  • To identify potential therapeutic targets for overcoming chemotherapy resistance.

Main Methods:

  • Flow cytometry to assess senescence-associated β-galactosidase (SA-β-gal) activity.
  • RNA sequencing (RNA-seq) to identify key senescence-regulating genes.
  • CBX7 knockdown and overexpression studies to evaluate its functional role.
  • Xenograft mouse models to validate in vivo effects.

Main Results:

  • Bortezomib (BTZ) induces myeloma cell senescence, with SA-β-gal activity correlated with proliferation.
  • CBX7 is a critical regulator of myeloma cell senescence, with levels fluctuating during disease course.
  • CBX7 knockdown promotes BTZ-induced senescence and growth arrest, while overexpression inhibits it.
  • CBX7 regulates senescence via the ERK/STAT3/MIX1 axis; targeting this pathway enhances BTZ efficacy.

Conclusions:

  • CBX7 is a pivotal regulator of cellular senescence in multiple myeloma.
  • A novel CBX7/ERK/PIM1 regulatory axis controls myeloma cell senescence.
  • Targeting CBX7 and its downstream pathways offers a strategy to augment standard chemotherapy efficacy in MM.
Keywords:
BortezomibCBX7Cellular senescenceMultiple myeloma

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