Sappanchalcone, a flavonoid isolated from Caesalpinia sappan L., induces caspase-dependent and AIF-dependent apoptosis in human colon cancer cells.

Abstract

The present study examined the apoptotic effects and the underlying mechanism of sappanchalcone, a major bioactive compound isolated from Caesalpinia sappan L. on human colon cancer cells. To achieve this, we used two different colon cancer cell lines, namely HCT116 (as wild-type p53 cells) and SW480 (as p53-mutant cells) cells. Our results illustrated that sappanchalcone treatment decreased the proliferation and further promoted apoptosis in HCT116 cells compared with the findings in SW480 cells. Sappanchalcone triggered phosphorylation of p53, which is involved in the activation of caspases and increased expression of Bax in HCT116 cells. Conversely, sappanchalcone-treated SW480 cells displayed no change in p53 phosphorylation or caspase activation. In addition, sappanchalcone further increased reactive oxygen species (ROS) levels and apoptosis-inducing factor (AIF) release in both HCT116 and SW480 cells. These data suggest that sappanchalcone induces apoptosis through caspase-dependent and caspases-independent mechanisms that were characterized by decreased Bcl-2 expression, mitochondrial targeting, and altered ROS production and AIF translocation to the nuclei.

• Authors: Hee Won Seo, Huiwon No, Hye Jin Cheon, Jin-Kyung Kim
• Journal: Chemico-biological interactions (Chem Biol Interact) Vol. 327 Pg. 109185 (Aug 25 2020) ISSN: 1872-7786 [Electronic] Ireland
• PMID: 32590072 (Publication Type: Journal Article)
• Copyright: Copyright © 2020 Elsevier B.V. All rights reserved.

Chemical References

• AIFM1 protein, human
• Apoptosis Inducing Factor
• Chalcones
• Reactive Oxygen Species
• TP53 protein, human
• Tumor Suppressor Protein p53
• sappanchalcone
• Caspases

Topics

• Apoptosis (drug effects)
• Apoptosis Inducing Factor (metabolism)
• Caspases (metabolism)
• Cell Nucleus (metabolism)
• Cell Proliferation (drug effects)
• Chalcones (pharmacology)
• Colonic Neoplasms (metabolism)
• Humans
• Membrane Potential, Mitochondrial (drug effects)
• Mitochondria (metabolism)
• Reactive Oxygen Species (metabolism)
• Tumor Suppressor Protein p53 (metabolism)