Synergistic anti-oral cancer effects of UVC and methanolic extracts of Cryptocarya concinna roots via apoptosis, oxidative stress and DNA damage

Hsueh Wei Chang, Jen Yang Tang, Ching Yu Yen, Hsun Shuo Chang, Hurng Wern Huang, Yi An Chung, Ih Sheng Chen, Ming Yii Huang

研究成果: 雜誌貢獻文章

4 引文 (Scopus)

摘要

Purpose Radiation combined with natural products may improve the radiosensitivity of cancer cells. This study investigated the potential of a combined modality treatment with Ultraviolet C (UVC; wavelength range 200–280 nm) and our previously identified anti-oral cancer agent (methanolic extracts of Cryptocarya concinna roots; MECCrt) in oral cancer cells. Materials and methods The mechanism of the possible synergy of UVC and MECCrt was explored in terms of cell viability, cell cycle, apoptosis, reactive oxygen species (ROS), mitochondrial membrane potential (MitoMP), and DNA damage analyses. Results In cell viability (%) at 24 h treatment, the low doses of UVC (14 J/m2) and MECCrt (10 μg/ml) resulted in slight damage to human oral cancer Ca9-22 cells (83.2 and 80.4) but was less harmful to human oral normal HGF-1 cells (93.4 and 91.8, respectively). The combined treatment of UVC and MECCrt (UVC/MECCrt) had a lower viability (54.5%) than UVC or MECCrt alone in Ca9-22 cells but no showed significant change in HGF-1 cells. In Ca9-22 cells, the expression of flow cytometry-based apoptosis (sub-G1 phase, annexin V, and pancaspase assays) was significantly higher in UVC/MECCrt than in UVC or MECCrt alone (p <0.0001). Using flow cytometry, intracellular ROS levels of UVC/MECCrt and MECCrt alone were higher than for UVC alone. MitoMP change and H2A histone family member X (γH2AX; H2AFX)-based DNA damage were synergistically inhibited and induced by MECCrt/UVC compared to its single treatment in Ca9-22 cells, respectively. Conclusion UVC plus MECCrt treatment had selective killing and synergistic anti-proliferative effects against oral cancer cells involving apoptosis, oxidative stress, and DNA damage. This combination therapy appears to have a great clinical potential against oral cancer cells.
原文英語
頁(從 - 到)1-10
頁數10
期刊International Journal of Radiation Biology
DOIs
出版狀態接受/付印 - 二月 17 2016

指紋

Cryptocarya
Mouth Neoplasms
DNA Damage
Oxidative Stress
Apoptosis
Mitochondrial Membrane Potential
Reactive Oxygen Species
Cell Survival
Flow Cytometry
Annexin A5
Radiation Tolerance
G1 Phase
Biological Products
Mitochondrial DNA
Histones

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging
  • Radiological and Ultrasound Technology

引用此文

Synergistic anti-oral cancer effects of UVC and methanolic extracts of Cryptocarya concinna roots via apoptosis, oxidative stress and DNA damage. / Chang, Hsueh Wei; Tang, Jen Yang; Yen, Ching Yu; Chang, Hsun Shuo; Huang, Hurng Wern; Chung, Yi An; Chen, Ih Sheng; Huang, Ming Yii.

於: International Journal of Radiation Biology, 17.02.2016, p. 1-10.

研究成果: 雜誌貢獻文章

Chang, Hsueh Wei ; Tang, Jen Yang ; Yen, Ching Yu ; Chang, Hsun Shuo ; Huang, Hurng Wern ; Chung, Yi An ; Chen, Ih Sheng ; Huang, Ming Yii. / Synergistic anti-oral cancer effects of UVC and methanolic extracts of Cryptocarya concinna roots via apoptosis, oxidative stress and DNA damage. 於: International Journal of Radiation Biology. 2016 ; 頁 1-10.
@article{d46e0b1689ff415985b77a6f80274625,
title = "Synergistic anti-oral cancer effects of UVC and methanolic extracts of Cryptocarya concinna roots via apoptosis, oxidative stress and DNA damage",
abstract = "Purpose Radiation combined with natural products may improve the radiosensitivity of cancer cells. This study investigated the potential of a combined modality treatment with Ultraviolet C (UVC; wavelength range 200–280 nm) and our previously identified anti-oral cancer agent (methanolic extracts of Cryptocarya concinna roots; MECCrt) in oral cancer cells. Materials and methods The mechanism of the possible synergy of UVC and MECCrt was explored in terms of cell viability, cell cycle, apoptosis, reactive oxygen species (ROS), mitochondrial membrane potential (MitoMP), and DNA damage analyses. Results In cell viability ({\%}) at 24 h treatment, the low doses of UVC (14 J/m2) and MECCrt (10 μg/ml) resulted in slight damage to human oral cancer Ca9-22 cells (83.2 and 80.4) but was less harmful to human oral normal HGF-1 cells (93.4 and 91.8, respectively). The combined treatment of UVC and MECCrt (UVC/MECCrt) had a lower viability (54.5{\%}) than UVC or MECCrt alone in Ca9-22 cells but no showed significant change in HGF-1 cells. In Ca9-22 cells, the expression of flow cytometry-based apoptosis (sub-G1 phase, annexin V, and pancaspase assays) was significantly higher in UVC/MECCrt than in UVC or MECCrt alone (p <0.0001). Using flow cytometry, intracellular ROS levels of UVC/MECCrt and MECCrt alone were higher than for UVC alone. MitoMP change and H2A histone family member X (γH2AX; H2AFX)-based DNA damage were synergistically inhibited and induced by MECCrt/UVC compared to its single treatment in Ca9-22 cells, respectively. Conclusion UVC plus MECCrt treatment had selective killing and synergistic anti-proliferative effects against oral cancer cells involving apoptosis, oxidative stress, and DNA damage. This combination therapy appears to have a great clinical potential against oral cancer cells.",
keywords = "apoptosis, DNA damage, mitochondrial membrane potential, natural products, oral cancer, ROS, Synergy, UVC",
author = "Chang, {Hsueh Wei} and Tang, {Jen Yang} and Yen, {Ching Yu} and Chang, {Hsun Shuo} and Huang, {Hurng Wern} and Chung, {Yi An} and Chen, {Ih Sheng} and Huang, {Ming Yii}",
year = "2016",
month = "2",
day = "17",
doi = "10.3109/09553002.2016.1145753",
language = "English",
pages = "1--10",
journal = "International Journal of Radiation Biology",
issn = "0955-3002",
publisher = "Informa Healthcare",

}

TY - JOUR

T1 - Synergistic anti-oral cancer effects of UVC and methanolic extracts of Cryptocarya concinna roots via apoptosis, oxidative stress and DNA damage

AU - Chang, Hsueh Wei

AU - Tang, Jen Yang

AU - Yen, Ching Yu

AU - Chang, Hsun Shuo

AU - Huang, Hurng Wern

AU - Chung, Yi An

AU - Chen, Ih Sheng

AU - Huang, Ming Yii

PY - 2016/2/17

Y1 - 2016/2/17

N2 - Purpose Radiation combined with natural products may improve the radiosensitivity of cancer cells. This study investigated the potential of a combined modality treatment with Ultraviolet C (UVC; wavelength range 200–280 nm) and our previously identified anti-oral cancer agent (methanolic extracts of Cryptocarya concinna roots; MECCrt) in oral cancer cells. Materials and methods The mechanism of the possible synergy of UVC and MECCrt was explored in terms of cell viability, cell cycle, apoptosis, reactive oxygen species (ROS), mitochondrial membrane potential (MitoMP), and DNA damage analyses. Results In cell viability (%) at 24 h treatment, the low doses of UVC (14 J/m2) and MECCrt (10 μg/ml) resulted in slight damage to human oral cancer Ca9-22 cells (83.2 and 80.4) but was less harmful to human oral normal HGF-1 cells (93.4 and 91.8, respectively). The combined treatment of UVC and MECCrt (UVC/MECCrt) had a lower viability (54.5%) than UVC or MECCrt alone in Ca9-22 cells but no showed significant change in HGF-1 cells. In Ca9-22 cells, the expression of flow cytometry-based apoptosis (sub-G1 phase, annexin V, and pancaspase assays) was significantly higher in UVC/MECCrt than in UVC or MECCrt alone (p <0.0001). Using flow cytometry, intracellular ROS levels of UVC/MECCrt and MECCrt alone were higher than for UVC alone. MitoMP change and H2A histone family member X (γH2AX; H2AFX)-based DNA damage were synergistically inhibited and induced by MECCrt/UVC compared to its single treatment in Ca9-22 cells, respectively. Conclusion UVC plus MECCrt treatment had selective killing and synergistic anti-proliferative effects against oral cancer cells involving apoptosis, oxidative stress, and DNA damage. This combination therapy appears to have a great clinical potential against oral cancer cells.

AB - Purpose Radiation combined with natural products may improve the radiosensitivity of cancer cells. This study investigated the potential of a combined modality treatment with Ultraviolet C (UVC; wavelength range 200–280 nm) and our previously identified anti-oral cancer agent (methanolic extracts of Cryptocarya concinna roots; MECCrt) in oral cancer cells. Materials and methods The mechanism of the possible synergy of UVC and MECCrt was explored in terms of cell viability, cell cycle, apoptosis, reactive oxygen species (ROS), mitochondrial membrane potential (MitoMP), and DNA damage analyses. Results In cell viability (%) at 24 h treatment, the low doses of UVC (14 J/m2) and MECCrt (10 μg/ml) resulted in slight damage to human oral cancer Ca9-22 cells (83.2 and 80.4) but was less harmful to human oral normal HGF-1 cells (93.4 and 91.8, respectively). The combined treatment of UVC and MECCrt (UVC/MECCrt) had a lower viability (54.5%) than UVC or MECCrt alone in Ca9-22 cells but no showed significant change in HGF-1 cells. In Ca9-22 cells, the expression of flow cytometry-based apoptosis (sub-G1 phase, annexin V, and pancaspase assays) was significantly higher in UVC/MECCrt than in UVC or MECCrt alone (p <0.0001). Using flow cytometry, intracellular ROS levels of UVC/MECCrt and MECCrt alone were higher than for UVC alone. MitoMP change and H2A histone family member X (γH2AX; H2AFX)-based DNA damage were synergistically inhibited and induced by MECCrt/UVC compared to its single treatment in Ca9-22 cells, respectively. Conclusion UVC plus MECCrt treatment had selective killing and synergistic anti-proliferative effects against oral cancer cells involving apoptosis, oxidative stress, and DNA damage. This combination therapy appears to have a great clinical potential against oral cancer cells.

KW - apoptosis

KW - DNA damage

KW - mitochondrial membrane potential

KW - natural products

KW - oral cancer

KW - ROS

KW - Synergy

KW - UVC

UR - http://www.scopus.com/inward/record.url?scp=84958745346&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84958745346&partnerID=8YFLogxK

U2 - 10.3109/09553002.2016.1145753

DO - 10.3109/09553002.2016.1145753

M3 - Article

C2 - 26887975

AN - SCOPUS:84958745346

SP - 1

EP - 10

JO - International Journal of Radiation Biology

JF - International Journal of Radiation Biology

SN - 0955-3002

ER -