Demethoxycurcumin in combination with ultraviolet radiation B induces apoptosis through the mitochondrial pathway and caspase activation in A431 and HaCaT cells

Photodynamic therapy is widely used in the clinical treatment of tumors, especially skin cancers. It has been reported that the photosensitizer curcumin, in combination with ultraviolet radiation B, induces HaCaT cell apoptosis, and this effect may be due to the activation of caspase pathways. In th...

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Main Authors: Yong Xin, Qian Huang, Pei Zhang, Wen Wen Guo, Long Zhen Zhang, Guan Jiang
Format: Article
Language:English
Published: SAGE Publishing 2017-05-01
Series:Tumor Biology
Online Access:https://doi.org/10.1177/1010428317706216
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author Yong Xin
Qian Huang
Pei Zhang
Wen Wen Guo
Long Zhen Zhang
Guan Jiang
author_facet Yong Xin
Qian Huang
Pei Zhang
Wen Wen Guo
Long Zhen Zhang
Guan Jiang
author_sort Yong Xin
collection DOAJ
description Photodynamic therapy is widely used in the clinical treatment of tumors, especially skin cancers. It has been reported that the photosensitizer curcumin, in combination with ultraviolet radiation B, induces HaCaT cell apoptosis, and this effect may be due to the activation of caspase pathways. In this study, we examined the photodynamic effects of demethoxycurcumin, a more stable analogue of curcumin, to determine whether it could induce apoptosis in skin cancer cells. We investigated the effects of a combination of ultraviolet radiation B and demethoxycurcumin on apoptotic cell death in A431 and HaCaT cells and determined the molecular mechanism of action. Our results showed increased apoptosis with a combination of ultraviolet radiation B with demethoxycurcumin, as compared to ultraviolet radiation B or demethoxycurcumin alone. The combination of ultraviolet radiation B irradiation with demethoxycurcumin synergistically induced apoptotic cell death in A431 and HaCaT cells through activation of p53 and caspase pathways, as well as through upregulation of Bax and p-p65 expression and downregulation of Bcl-2, Mcl-1, and nuclear factor-κB expression. In addition, we found that reactive oxygen species significantly increased with treatment, and mitochondrial membrane potential depolarization was remarkably enhanced. In conclusion, our data indicate that demethoxycurcumin may be a promising photosensitizer for use in photodynamic therapy to induce apoptosis in skin cancer cells.
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institution Kabale University
issn 1423-0380
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series Tumor Biology
spelling doaj-art-351311eb8bc84f4faf2142a0070eee282025-08-20T03:32:57ZengSAGE PublishingTumor Biology1423-03802017-05-013910.1177/1010428317706216Demethoxycurcumin in combination with ultraviolet radiation B induces apoptosis through the mitochondrial pathway and caspase activation in A431 and HaCaT cellsYong Xin0Qian Huang1Pei Zhang2Wen Wen Guo3Long Zhen Zhang4Guan Jiang5Department of Radiotherapy, Affiliated Hospital of Xuzhou Medical College, Xuzhou, ChinaDepartment of Radiotherapy, Affiliated Hospital of Xuzhou Medical College, Xuzhou, ChinaDepartment of Radiotherapy, Affiliated Hospital of Xuzhou Medical College, Xuzhou, ChinaDepartment of Radiotherapy, Affiliated Hospital of Xuzhou Medical College, Xuzhou, ChinaDepartment of Radiotherapy, Affiliated Hospital of Xuzhou Medical College, Xuzhou, ChinaDepartment of Dermatology, Affiliated Hospital of Xuzhou Medical College, Xuzhou, ChinaPhotodynamic therapy is widely used in the clinical treatment of tumors, especially skin cancers. It has been reported that the photosensitizer curcumin, in combination with ultraviolet radiation B, induces HaCaT cell apoptosis, and this effect may be due to the activation of caspase pathways. In this study, we examined the photodynamic effects of demethoxycurcumin, a more stable analogue of curcumin, to determine whether it could induce apoptosis in skin cancer cells. We investigated the effects of a combination of ultraviolet radiation B and demethoxycurcumin on apoptotic cell death in A431 and HaCaT cells and determined the molecular mechanism of action. Our results showed increased apoptosis with a combination of ultraviolet radiation B with demethoxycurcumin, as compared to ultraviolet radiation B or demethoxycurcumin alone. The combination of ultraviolet radiation B irradiation with demethoxycurcumin synergistically induced apoptotic cell death in A431 and HaCaT cells through activation of p53 and caspase pathways, as well as through upregulation of Bax and p-p65 expression and downregulation of Bcl-2, Mcl-1, and nuclear factor-κB expression. In addition, we found that reactive oxygen species significantly increased with treatment, and mitochondrial membrane potential depolarization was remarkably enhanced. In conclusion, our data indicate that demethoxycurcumin may be a promising photosensitizer for use in photodynamic therapy to induce apoptosis in skin cancer cells.https://doi.org/10.1177/1010428317706216
spellingShingle Yong Xin
Qian Huang
Pei Zhang
Wen Wen Guo
Long Zhen Zhang
Guan Jiang
Demethoxycurcumin in combination with ultraviolet radiation B induces apoptosis through the mitochondrial pathway and caspase activation in A431 and HaCaT cells
Tumor Biology
title Demethoxycurcumin in combination with ultraviolet radiation B induces apoptosis through the mitochondrial pathway and caspase activation in A431 and HaCaT cells
title_full Demethoxycurcumin in combination with ultraviolet radiation B induces apoptosis through the mitochondrial pathway and caspase activation in A431 and HaCaT cells
title_fullStr Demethoxycurcumin in combination with ultraviolet radiation B induces apoptosis through the mitochondrial pathway and caspase activation in A431 and HaCaT cells
title_full_unstemmed Demethoxycurcumin in combination with ultraviolet radiation B induces apoptosis through the mitochondrial pathway and caspase activation in A431 and HaCaT cells
title_short Demethoxycurcumin in combination with ultraviolet radiation B induces apoptosis through the mitochondrial pathway and caspase activation in A431 and HaCaT cells
title_sort demethoxycurcumin in combination with ultraviolet radiation b induces apoptosis through the mitochondrial pathway and caspase activation in a431 and hacat cells
url https://doi.org/10.1177/1010428317706216
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