Plectalibertellenone A suppresses colorectal cancer cell motility and glucose metabolism by targeting TGF-β/Smad and Wnt pathways

Chathurika D.B. Gamage, Jeong Hyeon Kim, Rui Zhou, So Yeon Park, Sultan Pulat, Mücahit Varlı, Sang Jip Nam, Hangun Kim

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

Colorectal cancer (CRC) is the second most common cause of cancer-related death and represents a serious worldwide health problem. CRC metastasis decreases the survival rate of cancer patients, underscoring the need to identify novel anticancer agents and therapeutic targets. Here, we introduce Plectalibertellenone A (B) as a promising agent for the inhibition of CRC cell motility and glucose metabolism and explore its mechanism of action in CRC cells. Plectalibertellenone A suppressed TGF-β gene expression and the activation of the TGF-β/Smad signaling pathway, leading to reverse epithelial to mesenchymal transition (EMT) by modulating the expressions of EMT markers and transcriptional factors such as E-cadherin, N-cadherin, vimentin, Slug, Snail, Twist, and ZEB1/2. Furthermore, disruption of Wnt signaling inhibited CRC motility and glucose metabolism including glycolysis and oxidative phosphorylation, primarily affecting glycolytic enzymes, GLUT1, HK2, PKM2, LDHA, and HIF-1α under hypoxic condition. Therefore, Plectalibertellenone A is a potential drug candidate that can be developed into a promising anticancer treatment to prevent CRC metastasis and inhibit glucose metabolism.

Original languageEnglish
Article numbere2120
JournalBioFactors
Volume51
Issue number1
DOIs
StatePublished - 1 Jan 2025

Bibliographical note

Publisher Copyright:
© 2024 International Union of Biochemistry and Molecular Biology.

Keywords

  • CRC
  • EMT
  • Plectalibertellenone A (B)
  • aerobic glycolysis
  • motility
  • oxidative phosphorylation

Fingerprint

Dive into the research topics of 'Plectalibertellenone A suppresses colorectal cancer cell motility and glucose metabolism by targeting TGF-β/Smad and Wnt pathways'. Together they form a unique fingerprint.

Cite this