UVA Irradiation Enhances Brusatol-Mediated Inhibition of Melanoma Growth by Downregulation of the Nrf2-Mediated Antioxidant Response
Brusatol (BR) is a potent inhibitor of Nrf2, a transcription factor that is highly expressed in cancer tissues and confers chemoresistance. UVA-generated reactive oxygen species (ROS) can damage both normal and cancer cells and may be of potential use in phototherapy. In order to provide an alternat...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2018-01, Vol.2018 (2018), p.1-15 |
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| creator | Bartsch, Jörg W. Ji, Ping Zhong, Julia Li Huang, Xiao Li, Wei Wu, Yan Guo, Yingying Nisar, Muhammad Farrukh Bian, Chunxiang Shi, Guangwei Wang, Mei Jiang, Xuemei |
| description | Brusatol (BR) is a potent inhibitor of Nrf2, a transcription factor that is highly expressed in cancer tissues and confers chemoresistance. UVA-generated reactive oxygen species (ROS) can damage both normal and cancer cells and may be of potential use in phototherapy. In order to provide an alternative method to treat the aggressive melanoma, we sought to investigate whether low-dose UVA with BR is more effective in eliminating melanoma cells than the respective single treatments. We found that BR combined with UVA led to inhibition of A375 melanoma cell proliferation by cell cycle arrest in the G1 phase and triggers cell apoptosis. Furthermore, inhibition of Nrf2 expression attenuated colony formation and tumor development from A375 cells in heterotopic mouse models. In addition, cotreatment of UVA and BR partially suppressed Nrf2 and its downstream target genes such as HO-1 along with the PI3K/AKT pathway. We propose that cotreatment increased ROS-induced cell cycle arrest and cellular apoptosis and inhibits melanoma growth by regulating the AKT-Nrf2 pathway in A375 cells which offers a possible therapeutic intervention strategy for the treatment of human melanoma. |
| doi_str_mv | 10.1155/2018/9742154 |
| format | Article |
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UVA-generated reactive oxygen species (ROS) can damage both normal and cancer cells and may be of potential use in phototherapy. In order to provide an alternative method to treat the aggressive melanoma, we sought to investigate whether low-dose UVA with BR is more effective in eliminating melanoma cells than the respective single treatments. We found that BR combined with UVA led to inhibition of A375 melanoma cell proliferation by cell cycle arrest in the G1 phase and triggers cell apoptosis. Furthermore, inhibition of Nrf2 expression attenuated colony formation and tumor development from A375 cells in heterotopic mouse models. In addition, cotreatment of UVA and BR partially suppressed Nrf2 and its downstream target genes such as HO-1 along with the PI3K/AKT pathway. We propose that cotreatment increased ROS-induced cell cycle arrest and cellular apoptosis and inhibits melanoma growth by regulating the AKT-Nrf2 pathway in A375 cells which offers a possible therapeutic intervention strategy for the treatment of human melanoma.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2018/9742154</identifier><identifier>PMID: 29670684</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Antioxidants ; Antioxidants - metabolism ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - radiation effects ; Cancer ; Care and treatment ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell Proliferation - radiation effects ; Development and progression ; Dose-Response Relationship, Radiation ; Down-Regulation - drug effects ; Down-Regulation - radiation effects ; Gene Knockout Techniques ; Humans ; Inactivation, Metabolic - drug effects ; Inactivation, Metabolic - radiation effects ; Ionizing radiation ; Kinases ; Melanoma ; Melanoma - drug therapy ; Melanoma - pathology ; Mice, Nude ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; Phototherapy ; Prevention ; Proto-Oncogene Proteins c-akt - metabolism ; Quassins - pharmacology ; Quassins - therapeutic use ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Rodents ; Signal Transduction ; Skin cancer ; Ultraviolet Rays</subject><ispartof>Oxidative medicine and cellular longevity, 2018-01, Vol.2018 (2018), p.1-15</ispartof><rights>Copyright © 2018 Mei Wang et al.</rights><rights>COPYRIGHT 2018 John Wiley & Sons, Inc.</rights><rights>Copyright © 2018 Mei Wang et al.; This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2018 Mei Wang et al. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-bf63b2d22d40540b68280b4989471a68f82ea141b8d24e126368a049b4f191163</citedby><cites>FETCH-LOGICAL-c499t-bf63b2d22d40540b68280b4989471a68f82ea141b8d24e126368a049b4f191163</cites><orcidid>0000-0001-8997-6824 ; 0000-0002-5799-3125</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835260/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5835260/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29670684$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Huang, Peng</contributor><creatorcontrib>Bartsch, Jörg W.</creatorcontrib><creatorcontrib>Ji, Ping</creatorcontrib><creatorcontrib>Zhong, Julia Li</creatorcontrib><creatorcontrib>Huang, Xiao</creatorcontrib><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Wu, Yan</creatorcontrib><creatorcontrib>Guo, Yingying</creatorcontrib><creatorcontrib>Nisar, Muhammad Farrukh</creatorcontrib><creatorcontrib>Bian, Chunxiang</creatorcontrib><creatorcontrib>Shi, Guangwei</creatorcontrib><creatorcontrib>Wang, Mei</creatorcontrib><creatorcontrib>Jiang, Xuemei</creatorcontrib><title>UVA Irradiation Enhances Brusatol-Mediated Inhibition of Melanoma Growth by Downregulation of the Nrf2-Mediated Antioxidant Response</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Brusatol (BR) is a potent inhibitor of Nrf2, a transcription factor that is highly expressed in cancer tissues and confers chemoresistance. UVA-generated reactive oxygen species (ROS) can damage both normal and cancer cells and may be of potential use in phototherapy. In order to provide an alternative method to treat the aggressive melanoma, we sought to investigate whether low-dose UVA with BR is more effective in eliminating melanoma cells than the respective single treatments. We found that BR combined with UVA led to inhibition of A375 melanoma cell proliferation by cell cycle arrest in the G1 phase and triggers cell apoptosis. Furthermore, inhibition of Nrf2 expression attenuated colony formation and tumor development from A375 cells in heterotopic mouse models. In addition, cotreatment of UVA and BR partially suppressed Nrf2 and its downstream target genes such as HO-1 along with the PI3K/AKT pathway. We propose that cotreatment increased ROS-induced cell cycle arrest and cellular apoptosis and inhibits melanoma growth by regulating the AKT-Nrf2 pathway in A375 cells which offers a possible therapeutic intervention strategy for the treatment of human melanoma.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Antioxidants - metabolism</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - radiation effects</subject><subject>Cancer</subject><subject>Care and treatment</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Proliferation - radiation effects</subject><subject>Development and progression</subject><subject>Dose-Response Relationship, Radiation</subject><subject>Down-Regulation - drug effects</subject><subject>Down-Regulation - radiation effects</subject><subject>Gene Knockout Techniques</subject><subject>Humans</subject><subject>Inactivation, Metabolic - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bartsch, Jörg W.</au><au>Ji, Ping</au><au>Zhong, Julia Li</au><au>Huang, Xiao</au><au>Li, Wei</au><au>Wu, Yan</au><au>Guo, Yingying</au><au>Nisar, Muhammad Farrukh</au><au>Bian, Chunxiang</au><au>Shi, Guangwei</au><au>Wang, Mei</au><au>Jiang, Xuemei</au><au>Huang, Peng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>UVA Irradiation Enhances Brusatol-Mediated Inhibition of Melanoma Growth by Downregulation of the Nrf2-Mediated Antioxidant Response</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>2018</volume><issue>2018</issue><spage>1</spage><epage>15</epage><pages>1-15</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Brusatol (BR) is a potent inhibitor of Nrf2, a transcription factor that is highly expressed in cancer tissues and confers chemoresistance. UVA-generated reactive oxygen species (ROS) can damage both normal and cancer cells and may be of potential use in phototherapy. In order to provide an alternative method to treat the aggressive melanoma, we sought to investigate whether low-dose UVA with BR is more effective in eliminating melanoma cells than the respective single treatments. We found that BR combined with UVA led to inhibition of A375 melanoma cell proliferation by cell cycle arrest in the G1 phase and triggers cell apoptosis. Furthermore, inhibition of Nrf2 expression attenuated colony formation and tumor development from A375 cells in heterotopic mouse models. In addition, cotreatment of UVA and BR partially suppressed Nrf2 and its downstream target genes such as HO-1 along with the PI3K/AKT pathway. We propose that cotreatment increased ROS-induced cell cycle arrest and cellular apoptosis and inhibits melanoma growth by regulating the AKT-Nrf2 pathway in A375 cells which offers a possible therapeutic intervention strategy for the treatment of human melanoma.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>29670684</pmid><doi>10.1155/2018/9742154</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0001-8997-6824</orcidid><orcidid>https://orcid.org/0000-0002-5799-3125</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Open Access; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection; PubMed Central Open Access |
| subjects | Animals Antioxidants Antioxidants - metabolism Apoptosis Apoptosis - drug effects Apoptosis - radiation effects Cancer Care and treatment Cell growth Cell Line, Tumor Cell Proliferation - drug effects Cell Proliferation - radiation effects Development and progression Dose-Response Relationship, Radiation Down-Regulation - drug effects Down-Regulation - radiation effects Gene Knockout Techniques Humans Inactivation, Metabolic - drug effects Inactivation, Metabolic - radiation effects Ionizing radiation Kinases Melanoma Melanoma - drug therapy Melanoma - pathology Mice, Nude NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism Phototherapy Prevention Proto-Oncogene Proteins c-akt - metabolism Quassins - pharmacology Quassins - therapeutic use Reactive oxygen species Reactive Oxygen Species - metabolism Rodents Signal Transduction Skin cancer Ultraviolet Rays |
| title | UVA Irradiation Enhances Brusatol-Mediated Inhibition of Melanoma Growth by Downregulation of the Nrf2-Mediated Antioxidant Response |
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