The Citrus Flavanone Hesperetin Induces Apoptosis in CTCL Cells


Journal

Anti-cancer agents in medicinal chemistry
ISSN: 1875-5992
Titre abrégé: Anticancer Agents Med Chem
Pays: Netherlands
ID NLM: 101265649

Informations de publication

Date de publication:
2020
Historique:
received: 01 12 2019
revised: 20 01 2020
accepted: 07 02 2020
pubmed: 26 3 2020
medline: 2 6 2021
entrez: 26 3 2020
Statut: ppublish

Résumé

Hesperetin is a natural compound known for its cholesterol-lowering effect and a wide range of pharmacological activities. Investigating the potential anticancer activities of Hesperetin in malignant hematolymphoid cell lines HuT78 and MJ, derived from patients with Cutaneous T-Cell Lymphomas (CTCL). The cytotoxic effect of Hesperetin on two different CTCL cell lines, HuT78 and MJ, was assessed by MTS-based colorimetric assay. Apoptosis, cell cycle, ROS (Reactive Oxygen Species) and molecular analysis were performed using flow-cytometry and immunoblotting. Hesperetin-treated CTCL cells were arrested at the sub-G1 phase of cell cycle with the concomitant decrease in the expression of the cell cycle regulator protein cyclin B. In addition, the study found that the cellular treatment with Hesperetin caused an induction of apoptosis, which was independent of ROS generation. Hesperetin caused a significant decrease in the expression level of anti-apoptotic protein Bcl-xL and an increase in cleaved caspase-3 and PARP proteins in CTCL cells. Furthermore, Hesperetin treatment in CTCL cells down-regulated the expression of Notch1 and phosphorylation of STAT3 (Tyr705) and inhibited NFκBp65. This study highlights the anticancer properties of Hesperetin. Which induces apoptosis in CTCL cells via STAT3/Notch1/NFκB mediated signaling pathway, suggesting that further development of this novel class of flavonoid may contribute to new drug discovery for certain hematolymphoid malignancies.

Sections du résumé

BACKGROUND
Hesperetin is a natural compound known for its cholesterol-lowering effect and a wide range of pharmacological activities.
OBJECTIVES
Investigating the potential anticancer activities of Hesperetin in malignant hematolymphoid cell lines HuT78 and MJ, derived from patients with Cutaneous T-Cell Lymphomas (CTCL).
METHODS
The cytotoxic effect of Hesperetin on two different CTCL cell lines, HuT78 and MJ, was assessed by MTS-based colorimetric assay. Apoptosis, cell cycle, ROS (Reactive Oxygen Species) and molecular analysis were performed using flow-cytometry and immunoblotting.
RESULTS
Hesperetin-treated CTCL cells were arrested at the sub-G1 phase of cell cycle with the concomitant decrease in the expression of the cell cycle regulator protein cyclin B. In addition, the study found that the cellular treatment with Hesperetin caused an induction of apoptosis, which was independent of ROS generation. Hesperetin caused a significant decrease in the expression level of anti-apoptotic protein Bcl-xL and an increase in cleaved caspase-3 and PARP proteins in CTCL cells. Furthermore, Hesperetin treatment in CTCL cells down-regulated the expression of Notch1 and phosphorylation of STAT3 (Tyr705) and inhibited NFκBp65.
CONCLUSION
This study highlights the anticancer properties of Hesperetin. Which induces apoptosis in CTCL cells via STAT3/Notch1/NFκB mediated signaling pathway, suggesting that further development of this novel class of flavonoid may contribute to new drug discovery for certain hematolymphoid malignancies.

Identifiants

pubmed: 32208126
pii: ACAMC-EPUB-105437
doi: 10.2174/1871521409666200324110031
doi:

Substances chimiques

Antineoplastic Agents, Phytogenic 0
NF-kappa B 0
NOTCH1 protein, human 0
Receptor, Notch1 0
STAT3 Transcription Factor 0
STAT3 protein, human 0
Hesperidin E750O06Y6O
hesperetin Q9Q3D557F1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1459-1468

Informations de copyright

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

Auteurs

Amuthavalli Kottaiswamy (A)

VRR Institute of Biomedical Science, University of Madras, Chennai, India.

Atish Kizhakeyil (A)

Lee Kong Chian School of Medicine, Nanyang Technological University Singapore, Clinical Sciences Building, 11 Mandalay Road, Nanyang Ave, Singapore.

Abirami M Padmanaban (AM)

VRR Institute of Biomedical Science, University of Madras, Chennai, India.

Fathima B Mirza (FB)

VRR Institute of Biomedical Science, University of Madras, Chennai, India.

Venkatesh R Vijay (VR)

Lee Kong Chian School of Medicine, Nanyang Technological University Singapore, Clinical Sciences Building, 11 Mandalay Road, Nanyang Ave, Singapore.

Pin S Lee (PS)

Lee Kong Chian School of Medicine, Nanyang Technological University Singapore, Clinical Sciences Building, 11 Mandalay Road, Nanyang Ave, Singapore.

Navin K Verma (NK)

Lee Kong Chian School of Medicine, Nanyang Technological University Singapore, Clinical Sciences Building, 11 Mandalay Road, Nanyang Ave, Singapore.

Parkavi Kalaiselvan (P)

Chettinad Hospital and Research Institute, Chennai, India.

Shila Samuel (S)

VRR Institute of Biomedical Science, University of Madras, Chennai, India.

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Classifications MeSH