Dual inhibition of the TrkA and JAK2 pathways using entrectinib and pacritinib suppresses the growth and metastasis of HER2-positive and triple-negative breast cancers

Cancer Lett. 2024 Aug 10:597:217023. doi: 10.1016/j.canlet.2024.217023. Epub 2024 Jun 7.

Abstract

HER2-positive and triple-negative breast cancers (TNBC) are difficult to treat and associated with poor prognosis. Despite showing initial response, HER2-positive breast cancers often acquire resistance to HER2-targeted therapies, and TNBC lack effective therapies. To overcome these clinical challenges, we evaluated the therapeutic utility of co-targeting TrkA and JAK2/STAT3 pathways in these breast cancer subtypes. Here, we report the novel combination of FDA-approved TrkA inhibitors (Entrectinib or Larotrectinib) and JAK2 inhibitors (Pacritinib or Ruxolitinib) synergistically inhibited in vitro growth of HER2-positive breast cancer cells and TNBC cells. The Entrectinib-Pacritinib combination inhibited the breast cancer stem cell subpopulation, reduced expression of stemness genes, SOX2 and MYC, and induced apoptosis. The Entrectinib-Pacritinib combination suppressed orthotopic growth of HER2-positive Trastuzumab-refractory breast cancer xenografts and basal patient-derived xenograft (PDXs), reduced tumoral SOX2 and MYC, and induced apoptosis in both mouse models. The Entrectinib-Pacritinib combination inhibited overall metastatic burden, and brain and bone metastases of intracardially inoculated TNBC cells without toxicity. Together, our results demonstrate for the first time that co-inhibition of TrkA and JAK2 synergistically suppresses breast cancer growth and metastasis, thereby providing preclinical evidence that supports future clinical evaluations.

Keywords: Breast cancer; Breast cancer metastasis; Combined targeted therapy; JAK2; TrkA.

MeSH terms

  • Animals
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology
  • Apoptosis / drug effects
  • Benzamides* / pharmacology
  • Bridged-Ring Compounds
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Drug Synergism
  • Female
  • Humans
  • Indazoles / pharmacology
  • Janus Kinase 2* / antagonists & inhibitors
  • Janus Kinase 2* / metabolism
  • Mice
  • Mice, Nude
  • Protein Kinase Inhibitors / pharmacology
  • Pyrazoles / pharmacology
  • Pyrimidines* / pharmacology
  • Receptor, ErbB-2* / antagonists & inhibitors
  • Receptor, ErbB-2* / genetics
  • Receptor, ErbB-2* / metabolism
  • Receptor, trkA* / antagonists & inhibitors
  • Receptor, trkA* / genetics
  • Receptor, trkA* / metabolism
  • Signal Transduction / drug effects
  • Triple Negative Breast Neoplasms* / drug therapy
  • Triple Negative Breast Neoplasms* / metabolism
  • Triple Negative Breast Neoplasms* / pathology
  • Xenograft Model Antitumor Assays*

Substances

  • Janus Kinase 2
  • Benzamides
  • entrectinib
  • Pyrimidines
  • Receptor, ErbB-2
  • JAK2 protein, human
  • Receptor, trkA
  • ERBB2 protein, human
  • NTRK1 protein, human
  • Indazoles
  • Pyrazoles
  • 11-(2-pyrrolidin-1-ylethoxy)-14,19-dioxa-5,7,26-triazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8,10,12(27),16,21,23-decaene
  • Protein Kinase Inhibitors
  • Bridged-Ring Compounds