HIV-protease inhibitors potentiate the activity of carfilzomib in triple-negative breast cancer

Br J Cancer. 2024 Sep;131(5):918-930. doi: 10.1038/s41416-024-02774-9. Epub 2024 Jul 5.

Abstract

Background: Resistance to chemotherapy is a major problem in the treatment of patients with triple-negative breast cancer (TNBC). Preclinical data suggest that TNBC is dependent on proteasomes; however, clinical observations indicate that the efficacy of proteasome inhibitors in TNBC may be limited, suggesting the need for combination therapies.

Methods: We compared bortezomib and carfilzomib and their combinations with nelfinavir and lopinavir in TNBC cell lines and primary cells with regard to their cytotoxic activity, functional proteasome inhibition, and induction of the unfolded protein response (UPR). Furthermore, we evaluated the involvement of sXBP1, ABCB1, and ABCG2 in the cytotoxic activity of drug combinations.

Results: Carfilzomib, via proteasome β5 + β2 inhibition, is more cytotoxic in TNBC than bortezomib, which inhibits β5 + β1 proteasome subunits. The cytotoxicity of carfilzomib was significantly potentiated by nelfinavir or lopinavir. Carfilzomib with lopinavir induced endoplasmic reticulum stress and pro-apoptotic UPR through the accumulation of excess proteasomal substrate protein in TNBC in vitro. Moreover, lopinavir increased the intracellular availability of carfilzomib by inhibiting carfilzomib export from cells that express high levels and activity of ABCB1, but not ABCG2.

Conclusion: Proteasome inhibition by carfilzomib combined with nelfinavir/lopinavir represents a potential treatment option for TNBC, warranting further investigation.

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B / metabolism
  • ATP Binding Cassette Transporter, Subfamily G, Member 2* / antagonists & inhibitors
  • ATP Binding Cassette Transporter, Subfamily G, Member 2* / metabolism
  • Antineoplastic Combined Chemotherapy Protocols / pharmacology
  • Apoptosis / drug effects
  • Bortezomib* / pharmacology
  • Cell Line, Tumor
  • Drug Synergism*
  • Endoplasmic Reticulum Stress / drug effects
  • Female
  • HIV Protease Inhibitors* / pharmacology
  • Humans
  • Lopinavir* / pharmacology
  • Nelfinavir* / pharmacology
  • Neoplasm Proteins / antagonists & inhibitors
  • Neoplasm Proteins / metabolism
  • Oligopeptides* / pharmacology
  • Proteasome Inhibitors / pharmacology
  • Triple Negative Breast Neoplasms* / drug therapy
  • Triple Negative Breast Neoplasms* / pathology
  • Unfolded Protein Response* / drug effects
  • X-Box Binding Protein 1 / genetics
  • X-Box Binding Protein 1 / metabolism

Substances

  • carfilzomib
  • Oligopeptides
  • HIV Protease Inhibitors
  • Nelfinavir
  • Lopinavir
  • Bortezomib
  • ATP Binding Cassette Transporter, Subfamily G, Member 2
  • Proteasome Inhibitors
  • ABCB1 protein, human
  • ABCG2 protein, human
  • Neoplasm Proteins
  • X-Box Binding Protein 1
  • ATP Binding Cassette Transporter, Subfamily B
  • XBP1 protein, human