Inhibition of the Stromal p38MAPK/MK2 Pathway Limits Breast Cancer Metastases and Chemotherapy-Induced Bone Loss

Cancer Res. 2018 Oct 1;78(19):5618-5630. doi: 10.1158/0008-5472.CAN-18-0234. Epub 2018 Aug 9.

Abstract

The role of the stromal compartment in tumor progression is best illustrated in breast cancer bone metastases, where the stromal compartment supports tumor growth, albeit through poorly defined mechanisms. p38MAPKα is frequently expressed in tumor cells and surrounding stromal cells, and its expression levels correlate with poor prognosis. This observation led us to investigate whether inhibition of p38MAPKα could reduce breast cancer metastases in a clinically relevant model. Orally administered, small-molecule inhibitors of p38MAPKα or its downstream kinase MK2 each limited outgrowth of metastatic breast cancer cells in the bone and visceral organs. This effect was primarily mediated by inhibition of the p38MAPKα pathway within the stromal compartment. Beyond effectively limiting metastatic tumor growth, these inhibitors reduced tumor-associated and chemotherapy-induced bone loss, which is a devastating comorbidity that drastically affects quality of life for patients with cancer. These data underscore the vital role played by stromal-derived factors in tumor progression and identify the p38MAPK-MK2 pathway as a promising therapeutic target for metastatic disease and prevention of tumor-induced bone loss.Significance: Pharmacologically targeting the stromal p38MAPK-MK2 pathway limits metastatic breast cancer growth, preserves bone quality, and extends survival. Cancer Res; 78(19); 5618-30. ©2018 AACR.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Administration, Oral
  • Animals
  • Antineoplastic Agents / adverse effects*
  • Bone Neoplasms / secondary
  • Bone and Bones / drug effects*
  • Bone and Bones / pathology
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Cell Line, Tumor
  • Disease Progression
  • Drug Therapy
  • Female
  • HEK293 Cells
  • Humans
  • Induction Chemotherapy
  • Intracellular Signaling Peptides and Proteins / metabolism*
  • MAP Kinase Signaling System
  • Macrophages / metabolism
  • Mice
  • Neoplasm Metastasis
  • Osteoclasts / metabolism
  • Paclitaxel / pharmacology
  • Prognosis
  • Protein Serine-Threonine Kinases / metabolism*
  • Quality of Life
  • Stromal Cells / metabolism
  • Tumor Microenvironment
  • p38 Mitogen-Activated Protein Kinases / metabolism*

Substances

  • Antineoplastic Agents
  • Intracellular Signaling Peptides and Proteins
  • MAP-kinase-activated kinase 2
  • Protein Serine-Threonine Kinases
  • p38 Mitogen-Activated Protein Kinases
  • Paclitaxel