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Targeting Caveolin-1 in Multiple Myeloma Cells Enhances Chemotherapy and Natural Killer Cell-Mediated Immunotherapy

Dewen Zhan1,2, Zhimin Du3, Shang Zhang1,2

  • 1The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, 510130, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|December 4, 2024
PubMed

Insights

Caveolin-1 (CAV1) is highly expressed in multiple myeloma (MM) cells, driving drug resistance. Inhibiting CAV1 enhances chemotherapy and immunotherapy efficacy in MM by targeting MM cell vulnerabilities.

Area of Science:

  • Oncology
  • Cell Biology
  • Immunology

Background:

  • Multiple myeloma (MM) cell membrane transport and surface targets critically impact treatment outcomes.
  • Caveolin-1 (CAV1), a key component of lipid rafts, is upregulated in MM and linked to disease progression and therapeutic resistance.

Purpose of the Study:

  • To investigate the role of CAV1 in MM cell biology and its potential as a therapeutic target.
  • To evaluate the effects of CAV1 inhibition on MM cell drug resistance, immune cell-mediated cytotoxicity, and metabolic vulnerabilities.

Main Methods:

  • CAV1 knockdown and inhibition in MM cell lines and in vivo mouse models.
  • Assessment of MM cell adhesion, drug resistance (bortezomib), natural killer (NK) cell cytotoxicity, mitochondrial function, redox homeostasis, and glutamine metabolism.
  • Evaluation of CAV1 inhibition combined with FDA-approved drugs (6-mercaptopurine, daidzin, statins).

Main Results:

  • CAV1 knockdown reduced MM cell adhesion and bortezomib resistance.
  • CAV1 inhibition enhanced NK cell cytotoxicity via increased CXCL10, SLAMF7, and CD112 expression.
  • CAV1 suppression disrupted redox homeostasis, enhanced glutamine addiction (via ASCT2, LAT1), and increased sensitivity to starvation and glutamine deprivation.
  • CAV1 inhibition slowed tumor growth in vivo and sensitized MM cells to bortezomib.

Conclusions:

  • CAV1 is a significant therapeutic target in multiple myeloma.
  • Targeting CAV1 can overcome drug resistance, enhance immunotherapy, and disrupt MM cell metabolism, offering a promising strategy to improve patient outcomes.
Keywords:
caveolin‐1glutathione metabolismimmunotherapymultiple myelomanatural killer cellredox homeostasis

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