BRD4-specific PROTAC inhibits basal-like breast cancer partially through downregulating KLF5 expression

Yanjie Kong1, Tianlong Lan2, Luzhen Wang3

  • 1Pathology Department, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital, Shenzhen, China.

Oncogene
|August 20, 2024
PubMed

Insights

A novel proteolysis-targeting chimera (PROTAC) drug, 6b, specifically targets and degrades BRD4, inhibiting basal-like breast cancer (BLBC) growth by downregulating the KLF5 oncoprotein. This compound shows therapeutic potential for BLBC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • Proteolysis-targeting chimeras (PROTACs) are emerging as a promising cancer therapy strategy.
  • Bromodomain and extra terminal domain (BET) proteins, particularly BRD4, are implicated in basal-like breast cancer (BLBC) progression.
  • Existing BRD4 PROTACs face challenges with bioavailability, non-selective degradation, and poor tumor targeting.

Purpose of the Study:

  • To develop and evaluate a novel BRD4-specific PROTAC, compound 6b, for its efficacy against BLBC.
  • To investigate the mechanism of action of 6b, including its effects on BRD4, KLF5, and BLBC cell growth.
  • To assess the therapeutic potential of 6b in preclinical models of BLBC.

Main Methods:

  • Synthesis and characterization of compound 6b, a BRD4-targeting PROTAC.
  • In vitro assays to assess BRD4 degradation and inhibition of BLBC cell proliferation.
  • Analysis of KLF5 expression and its regulation by BRD4-mediated super-enhancers.
  • In vivo studies using a xenograft mouse model to evaluate tumor growth inhibition by 6b.
  • Combination studies with KLF5 inhibitors to assess additive effects.

Main Results:

  • Compound 6b selectively induced cereblon (CRBN)-mediated ubiquitination and proteasomal degradation of BRD4, without affecting BRD2 or BRD3.
  • 6b significantly suppressed BLBC cell growth and inhibited the expression of the oncoprotein Krüppel-like factor 5 (KLF5).
  • 6b demonstrated significant inhibition of HCC1806 tumor growth in a xenograft mouse model.
  • The combination of 6b and KLF5 inhibitors exhibited additive effects in BLBC models.

Conclusions:

  • BRD4-specific PROTACs, such as 6b, can effectively inhibit BLBC by downregulating KLF5.
  • Compound 6b demonstrates potent anti-BLBC activity and warrants further investigation as a novel therapeutic agent.
  • Targeting BRD4 with PROTACs offers a promising strategy for overcoming limitations of existing therapies in BLBC.

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