Harnessing the Power of Kiwifruit for Radiosensitization of Melanoma.


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
Dec 2021
Historique:
received: 29 09 2021
revised: 23 10 2021
accepted: 03 11 2021
entrez: 1 12 2021
pubmed: 2 12 2021
medline: 15 12 2021
Statut: ppublish

Résumé

Melanoma is the deadliest variant of skin cancer and its incidence continues to increase. There are limited treatment options for advanced and metastatic cases of melanoma, despite advances in immunotherapy and chemotherapy. Melanoma is notorious as a radioresistant tumor. Previous studies found that phytochemicals, such as resveratrol and those found in green tea and blueberry, can sensitize various cancer cells, including melanoma, to radiotherapy. Our previous study also revealed that kiwifruit extract (KE) has antitumor activity to melanoma cells. This study was designed to expand upon our previous investigation and determine KE's potential as a radiosensitizer on CRL-11147 melanoma cancer cells and elucidate the possible mechanisms behind its potential. Proliferation and apoptosis of CRL-11147 melanoma cells under radiation therapy (RT) plus KE versus RT alone were investigated using Proliferative cell nuclear antigen (PCNA) staining, quick cell proliferation assay, clonogenic assay, and caspase-3 activity assay. Reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC) were then used to investigate the mechanisms behind the observed results. The percentage of CRL-11147 colonies, PCNA staining intensity, and the optic density value of CRL-11147 cells decreased with RT/KE vs. RT alone. Relative caspase-3 activity was increased with RT/KE vs. RT alone. Increased expression of the anti-proliferative molecule p27 and pro-apoptotic molecule TRAILR1 correlated with the anti-tumor effect seen in the RT/KE group versus the RT alone group. KE augments radiosensitivity of CRL-11147 by up-regulating both p27 and TRAILR1 to inhibit proliferation and increase apoptosis, respectively.

Sections du résumé

BACKGROUND BACKGROUND
Melanoma is the deadliest variant of skin cancer and its incidence continues to increase. There are limited treatment options for advanced and metastatic cases of melanoma, despite advances in immunotherapy and chemotherapy. Melanoma is notorious as a radioresistant tumor. Previous studies found that phytochemicals, such as resveratrol and those found in green tea and blueberry, can sensitize various cancer cells, including melanoma, to radiotherapy. Our previous study also revealed that kiwifruit extract (KE) has antitumor activity to melanoma cells. This study was designed to expand upon our previous investigation and determine KE's potential as a radiosensitizer on CRL-11147 melanoma cancer cells and elucidate the possible mechanisms behind its potential.
MATERIALS AND METHODS METHODS
Proliferation and apoptosis of CRL-11147 melanoma cells under radiation therapy (RT) plus KE versus RT alone were investigated using Proliferative cell nuclear antigen (PCNA) staining, quick cell proliferation assay, clonogenic assay, and caspase-3 activity assay. Reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC) were then used to investigate the mechanisms behind the observed results.
RESULTS RESULTS
The percentage of CRL-11147 colonies, PCNA staining intensity, and the optic density value of CRL-11147 cells decreased with RT/KE vs. RT alone. Relative caspase-3 activity was increased with RT/KE vs. RT alone. Increased expression of the anti-proliferative molecule p27 and pro-apoptotic molecule TRAILR1 correlated with the anti-tumor effect seen in the RT/KE group versus the RT alone group.
CONCLUSION CONCLUSIONS
KE augments radiosensitivity of CRL-11147 by up-regulating both p27 and TRAILR1 to inhibit proliferation and increase apoptosis, respectively.

Identifiants

pubmed: 34848448
pii: 41/12/5945
doi: 10.21873/anticanres.15413
doi:

Substances chimiques

Plant Extracts 0
Radiation-Sensitizing Agents 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

5945-5951

Informations de copyright

Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Leon Kou (L)

HCA Healthcare/USF Morsani College of Medicine GME/St. Petersburg General Hospital, St. Petersburg, FL, U.S.A.
Department of Microbiology, Immunology & Pathology, Des Moines University College of Osteopathic Medicine, Des Moines, IA, U.S.A.

Ziwen Zhu (Z)

Department of Surgery, University of Missouri School of Medicine, Columbia, MO, U.S.A.

Emerson Fajardo (E)

Department of Surgery, University of Missouri School of Medicine, Columbia, MO, U.S.A.

Qian Bai (Q)

Department of Surgery, University of Missouri School of Medicine, Columbia, MO, U.S.A.

Chase Redington (C)

Department of Surgery, University of Missouri School of Medicine, Columbia, MO, U.S.A.

Huaping Xiao (H)

Department of Surgery, University of Missouri School of Medicine, Columbia, MO, U.S.A.

Marco Lequio (M)

Department of Microbiology, Immunology & Pathology, Des Moines University College of Osteopathic Medicine, Des Moines, IA, U.S.A.
Department of Surgery, University of Missouri School of Medicine, Columbia, MO, U.S.A.

Nelson Sham (N)

Department of Microbiology, Immunology & Pathology, Des Moines University College of Osteopathic Medicine, Des Moines, IA, U.S.A.

Mark R Wakefield (MR)

Department of Surgery, University of Missouri School of Medicine, Columbia, MO, U.S.A.

Yujiang Fang (Y)

Department of Microbiology, Immunology & Pathology, Des Moines University College of Osteopathic Medicine, Des Moines, IA, U.S.A.; yujiang.fang@dmu.edu.
Department of Surgery, University of Missouri School of Medicine, Columbia, MO, U.S.A.

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Classifications MeSH