A natural degradant of curcumin, feruloylacetone inhibits cell proliferation via inducing cell cycle arrest and a mitochondrial apoptotic pathway in hct116 colon cancer cells
Journal
Molecules
Journal Volume
26
Journal Issue
16
Date Issued
2021
Author(s)
Abstract
Feruloylacetone (FER) is a natural degradant of curcumin after heating, which structurally reserves some functional groups of curcumin. It is not as widely discussed as its original counterpart has been previously; and in this study, its anticancer efficacy is investigated. This study focuses on the suppressive effect of FER on colon cancer, as the efficacious effect of curcumin on this typical cancer type has been well evidenced. In addition, demethoxy-feruloylacetone (DFER) was applied to compare the effect that might be brought on by the structural differences of the methoxy group. It was revealed that both FER and DFER inhibited the proliferation of HCT116 cells, possibly via suppression of the phosphorylated mTOR/STAT3 pathway. Notably, FER could significantly repress both the STAT3 phosphorylation and protein levels. Furthermore, both samples showed capability of arresting HCT116 cells at the G2/M phase via the activation of p53/p21 and the upregulation of cyclin-B. In addition, ROS elevation and changes in mitochondrial membrane potential were revealed, as indicated by p-atm elevation. The apoptotic rate rose to 36.9 and 32.2% after being treated by FER and DFER, respectively. In summary, both compounds exhibited an anticancer effect, and FER showed a greater proapoptotic effect, possibly due to the presence of the methoxy group on the aromatic ring. ? 2021 by the authors. Licensee MDPI, Basel, Switzerland.
Subjects
Colon cancer
Curcumin
Degradant
Demethoxy-feruloylacetone
Feruloylacetone
antineoplastic agent
antioxidant
CCNB1 protein, human
CDKN1A protein, human
curcumin
cyclin B1
cyclin dependent kinase inhibitor 1A
feruloylacetone
MTOR protein, human
phenol
protein p53
reactive oxygen metabolite
STAT3 protein
STAT3 protein, human
styrene derivative
target of rapamycin kinase
apoptosis
cell cycle checkpoint
cell cycle G2 phase
cell division
cell proliferation
chemistry
colon tumor
drug effect
HCT 116 cell line
human
metabolism
mitochondrial membrane potential
mitochondrion
pathology
phosphorylation
Antineoplastic Agents
Antioxidants
Apoptosis
Cell Cycle Checkpoints
Cell Division
Cell Proliferation
Colonic Neoplasms
Cyclin B1
Cyclin-Dependent Kinase Inhibitor p21
G2 Phase
HCT116 Cells
Humans
Membrane Potential, Mitochondrial
Mitochondria
Phenol
Phosphorylation
Reactive Oxygen Species
STAT3 Transcription Factor
Styrenes
TOR Serine-Threonine Kinases
Tumor Suppressor Protein p53
SDGs
Type
journal article