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Targeting CCL2/CCR2 Signaling Overcomes MEK Inhibitor Resistance in Acute Myeloid Leukemia.

Rucha V Modak1,2,3,4, Katia G de Oliveira Rebola1,2,3,4, John McClatchy1,2,3,4

  • 1Division of Oncological Sciences, Oregon Health & Science University, Portland, Oregon.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|March 7, 2024
PubMed
Summary

Elevated CCL2 levels in acute myeloid leukemia (AML) confer resistance to MEK inhibitors (MEKi). Targeting the CCL2/CCR2 axis with MEKi combination therapy can overcome this resistance, improving AML treatment outcomes.

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Area of Science:

  • Hematology
  • Oncology
  • Molecular Biology

Background:

  • The tumor microenvironment influences acute myeloid leukemia (AML) progression and drug resistance.
  • Extrinsic factors protect leukemia cells, necessitating therapies targeting both intrinsic and extrinsic signaling pathways.

Purpose of the Study:

  • To investigate the role of extrinsic factors in mediating resistance to MEK inhibitors (MEKi) in AML.
  • To identify novel therapeutic strategies to overcome MEKi resistance in AML patients.

Main Methods:

  • Analysis of gene expression, secreted cytokines, and drug sensitivity in approximately 300 AML patient samples.
  • Validation of identified associations using loss-of-function and pharmacologic inhibition studies.
  • Global phosphoproteomics and CRISPR/Cas9 screening to elucidate mechanisms of resistance.

Main Results:

  • Elevated CCL2 levels were significantly associated with reduced sensitivity to MEKi.
  • CCL2 activates prosurvival pathways (MAPK, cell-cycle regulation) in MEKi-resistant AML cells.
  • Inhibition of the CCL2/CCR2 axis sensitized AML cells to trametinib, reducing proliferation and increasing apoptosis.

Conclusions:

  • CCL2/CCR2 signaling is a key mechanism of MEKi resistance in AML.
  • Combination therapy targeting the CCL2/CCR2 axis and MEK pathway shows promise for overcoming drug resistance.
  • This strategy may improve treatment efficacy and outcomes for AML patients.