Evacetrapib Elicits Antitumor Effects on Colorectal Cancer by Inhibiting the Wnt/β-Catenin Signaling Pathway and Activating the JNK Signaling Pathway

Biol Pharm Bull. 2022;45(9):1238-1245. doi: 10.1248/bpb.b22-00053.

Abstract

Despite advances in colorectal cancer (CRC) treatment, most advanced CRC patients who experience disease progression after chemotherapy, targeted therapy, and immunotherapy face a situation in which there is no available medicine. Thus, new therapeutic drugs for CRC are urgently needed. Studies have shown that cholesteryl ester transfer protein (CETP) has a vital role in tumor development and is a possible target for CRC therapy. We found that Evacetrapib, a CETP inhibitor, suppressed CRC cell growth by inhibiting the Wnt/β-catenin signaling pathway and activating the c-Jun NH2-terminal kinase (JNK) signaling pathway in CRC. Therefore, Evacetrapib displays an anti-cancer effect and is a possible option for treating CRC.

Keywords: Evacetrapib; Wnt; c-Jun NH2-terminal kinase; cholesteryl ester transfer protein; colorectal cancer; β-catenin.

MeSH terms

  • Benzodiazepines
  • Cell Line, Tumor
  • Cell Proliferation
  • Colorectal Neoplasms* / pathology
  • Gene Expression Regulation, Neoplastic
  • Humans
  • MAP Kinase Signaling System
  • Wnt Signaling Pathway*
  • beta Catenin / metabolism

Substances

  • beta Catenin
  • Benzodiazepines
  • evacetrapib