Combined Treatment of Sulfonyl Chromen-4-Ones (CHW09) and Ultraviolet-C (UVC) Enhances Proliferation Inhibition, Apoptosis, Oxidative Stress, and DNA Damage against Oral Cancer Cells
The sensitizing effect of chromone-derived compounds on UVC-induced proliferation inhibition has not been comprehensively investigated so far. The subject of this study was to examine the proliferation change of oral cancer cells while using the combined treatment of UVC (254 nm) with our previously...
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| description | The sensitizing effect of chromone-derived compounds on UVC-induced proliferation inhibition has not been comprehensively investigated so far. The subject of this study was to examine the proliferation change of oral cancer cells while using the combined treatment of UVC (254 nm) with our previously developed sulfonyl chromen-4-ones (CHW09), namely UVC/CHW09. Cell viability, apoptosis, oxidative stress, and DNA damage for the individual and combined treatments for UVC and/or CHW09 were examined in oral cancer Ca9-22 cells. In 24 h MTS assay, UVC (30 J/m
; UVC30), or CHW09 (25 and 50 µg/mL; namely, CHW09-25 and CHW09-50) show 54%, 59%, and 45% viability. The combined treatment (UVC30/CHW09-25 and UVC30/CHW09-50) show lower cell viability (45% and 35%). Mechanistically, UVC/CHW09 induced higher apoptosis than individual treatments and untreated control, which were supported by the evidence of flow cytometry for subG1, annexin V/7-aminoactinomycin D, pancaspase and caspases 3/7 activity, and western blotting for cleaved poly(ADP-ribose) polymerase. Moreover, this cleaved PARP expression was downregulated by pancaspase inhibitor Z-VAD-FMK. UVC/CHW09 showed higher oxidative stress than individual treatments and untreated control in terms of flow cytometry for reactive oxygen species, mitochondrial membrane potential, and mitochondrial mass. Furthermore, UVC/CHW09 showed higher DNA damage than individual treatments and untreated control in terms of flow cytometry for H2A histone family member X and 8-oxo-2'-deoxyguanosine. In conclusion, combined treatment UVC/CHW09 suppresses proliferation, and promotes apoptosis, oxidative stress, and DNA damage against oral cancer cells, providing a novel application of sulfonyl chromen-4-ones in order to sensitize UVC induced proliferation inhibition for oral cancer therapy. |
| doi_str_mv | 10.3390/ijms21176443 |
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; UVC30), or CHW09 (25 and 50 µg/mL; namely, CHW09-25 and CHW09-50) show 54%, 59%, and 45% viability. The combined treatment (UVC30/CHW09-25 and UVC30/CHW09-50) show lower cell viability (45% and 35%). Mechanistically, UVC/CHW09 induced higher apoptosis than individual treatments and untreated control, which were supported by the evidence of flow cytometry for subG1, annexin V/7-aminoactinomycin D, pancaspase and caspases 3/7 activity, and western blotting for cleaved poly(ADP-ribose) polymerase. Moreover, this cleaved PARP expression was downregulated by pancaspase inhibitor Z-VAD-FMK. UVC/CHW09 showed higher oxidative stress than individual treatments and untreated control in terms of flow cytometry for reactive oxygen species, mitochondrial membrane potential, and mitochondrial mass. Furthermore, UVC/CHW09 showed higher DNA damage than individual treatments and untreated control in terms of flow cytometry for H2A histone family member X and 8-oxo-2'-deoxyguanosine. In conclusion, combined treatment UVC/CHW09 suppresses proliferation, and promotes apoptosis, oxidative stress, and DNA damage against oral cancer cells, providing a novel application of sulfonyl chromen-4-ones in order to sensitize UVC induced proliferation inhibition for oral cancer therapy.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms21176443</identifier><identifier>PMID: 32899415</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Annexin V ; Apoptosis ; Cancer therapies ; Cell Cycle ; Cell growth ; Cell Movement ; Cell Proliferation ; Cell viability ; Chromones - chemistry ; Chromones - pharmacology ; Combined Modality Therapy ; Cytotoxicity ; Deoxyguanosine ; Deoxyribonucleic acid ; DNA ; DNA Damage ; Flow cytometry ; Humans ; Lung cancer ; Membrane potential ; Membrane Potential, Mitochondrial ; Mitochondria ; Mouth Neoplasms - drug therapy ; Mouth Neoplasms - metabolism ; Mouth Neoplasms - pathology ; Mouth Neoplasms - radiotherapy ; Oral cancer ; Oxidative Stress ; Poly (ADP-Ribose) Polymerase-1 - metabolism ; Poly(ADP-ribose) ; Poly(ADP-ribose) polymerase ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Ribose ; Tumor Cells, Cultured ; Ultraviolet Rays ; Western blotting</subject><ispartof>International journal of molecular sciences, 2020-09, Vol.21 (17), p.6443</ispartof><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2020 by the authors. 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c412t-6f3a31dcef9014d55f4dfba10bb9fcb06b1bbca7a0c17c13b908aebe739951193</citedby><cites>FETCH-LOGICAL-c412t-6f3a31dcef9014d55f4dfba10bb9fcb06b1bbca7a0c17c13b908aebe739951193</cites><orcidid>0000-0002-1983-8570 ; 0000-0002-4753-788X ; 0000-0003-0068-2366 ; 0000-0002-5690-0708</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/PMC7504536/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7504536/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32899415$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Sheng-Chieh</creatorcontrib><creatorcontrib>Wang, Yen-Yun</creatorcontrib><creatorcontrib>Lin, Li-Ching</creatorcontrib><creatorcontrib>Chang, Meng-Yang</creatorcontrib><creatorcontrib>Yuan, Shyng-Shiou F</creatorcontrib><creatorcontrib>Tang, Jen-Yang</creatorcontrib><creatorcontrib>Chang, Hsueh-Wei</creatorcontrib><title>Combined Treatment of Sulfonyl Chromen-4-Ones (CHW09) and Ultraviolet-C (UVC) Enhances Proliferation Inhibition, Apoptosis, Oxidative Stress, and DNA Damage against Oral Cancer Cells</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>The sensitizing effect of chromone-derived compounds on UVC-induced proliferation inhibition has not been comprehensively investigated so far. The subject of this study was to examine the proliferation change of oral cancer cells while using the combined treatment of UVC (254 nm) with our previously developed sulfonyl chromen-4-ones (CHW09), namely UVC/CHW09. Cell viability, apoptosis, oxidative stress, and DNA damage for the individual and combined treatments for UVC and/or CHW09 were examined in oral cancer Ca9-22 cells. In 24 h MTS assay, UVC (30 J/m
; UVC30), or CHW09 (25 and 50 µg/mL; namely, CHW09-25 and CHW09-50) show 54%, 59%, and 45% viability. The combined treatment (UVC30/CHW09-25 and UVC30/CHW09-50) show lower cell viability (45% and 35%). Mechanistically, UVC/CHW09 induced higher apoptosis than individual treatments and untreated control, which were supported by the evidence of flow cytometry for subG1, annexin V/7-aminoactinomycin D, pancaspase and caspases 3/7 activity, and western blotting for cleaved poly(ADP-ribose) polymerase. Moreover, this cleaved PARP expression was downregulated by pancaspase inhibitor Z-VAD-FMK. UVC/CHW09 showed higher oxidative stress than individual treatments and untreated control in terms of flow cytometry for reactive oxygen species, mitochondrial membrane potential, and mitochondrial mass. Furthermore, UVC/CHW09 showed higher DNA damage than individual treatments and untreated control in terms of flow cytometry for H2A histone family member X and 8-oxo-2'-deoxyguanosine. In conclusion, combined treatment UVC/CHW09 suppresses proliferation, and promotes apoptosis, oxidative stress, and DNA damage against oral cancer cells, providing a novel application of sulfonyl chromen-4-ones in order to sensitize UVC induced proliferation inhibition for oral cancer therapy.</description><subject>Annexin V</subject><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>Cell Cycle</subject><subject>Cell growth</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cell viability</subject><subject>Chromones - chemistry</subject><subject>Chromones - pharmacology</subject><subject>Combined Modality Therapy</subject><subject>Cytotoxicity</subject><subject>Deoxyguanosine</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>Flow cytometry</subject><subject>Humans</subject><subject>Lung cancer</subject><subject>Membrane potential</subject><subject>Membrane Potential, Mitochondrial</subject><subject>Mitochondria</subject><subject>Mouth Neoplasms - drug therapy</subject><subject>Mouth Neoplasms - metabolism</subject><subject>Mouth Neoplasms - pathology</subject><subject>Mouth Neoplasms - radiotherapy</subject><subject>Oral cancer</subject><subject>Oxidative Stress</subject><subject>Poly (ADP-Ribose) Polymerase-1 - metabolism</subject><subject>Poly(ADP-ribose)</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Ribose</subject><subject>Tumor Cells, Cultured</subject><subject>Ultraviolet Rays</subject><subject>Western blotting</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpVkUFr2zAYhsXYWLtut52HYJcW4k2yZDu6FILbroWyDNpsR_PJlhIFWcokJax_bL-vCu1KdtLHp4dHr3gR-kjJF8YE-WrWYywpbWrO2St0THlZFoTUzeuD-Qi9i3FNSMnKSrxFR6ycCsFpdYz-tn6UxqkB3wcFaVQuYa_x3dZq7x4sblfB52XBi7lTEZ-217-IOMPgBrywKcDOeKtS0eLTxc_2DF-6Fbg-gz-Ct0arAMl4h2_cykizHyd4tvGb5KOJEzz_Y4YM7BS-S0HFvNl7L77P8AWMsFQYlmBcTHgeIEfZmwNulbXxPXqjwUb14fk8QYury_v2uridf7tpZ7dFz2mZilozYHTolRaE8qGqNB-0BEqkFLqXpJZUyh4aID1tesqkIFNQUjVMiIpSwU7Q-ZN3s5WjyiKX_2y7TTAjhIfOg-n-v3Fm1S39rmsqwitWZ8HnZ0Hwv7cqpm7tt8HlzF3JOWkqwaZNpiZPVB98jEHplxco6fYtd4ctZ_zTYaoX-F-t7BHnR6Vz</recordid><startdate>20200903</startdate><enddate>20200903</enddate><creator>Wang, Sheng-Chieh</creator><creator>Wang, Yen-Yun</creator><creator>Lin, Li-Ching</creator><creator>Chang, Meng-Yang</creator><creator>Yuan, Shyng-Shiou F</creator><creator>Tang, Jen-Yang</creator><creator>Chang, Hsueh-Wei</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1983-8570</orcidid><orcidid>https://orcid.org/0000-0002-4753-788X</orcidid><orcidid>https://orcid.org/0000-0003-0068-2366</orcidid><orcidid>https://orcid.org/0000-0002-5690-0708</orcidid></search><sort><creationdate>20200903</creationdate><title>Combined Treatment of Sulfonyl Chromen-4-Ones (CHW09) and Ultraviolet-C (UVC) Enhances Proliferation Inhibition, Apoptosis, Oxidative Stress, and DNA Damage against Oral Cancer Cells</title><author>Wang, Sheng-Chieh ; Wang, Yen-Yun ; Lin, Li-Ching ; Chang, Meng-Yang ; Yuan, Shyng-Shiou F ; Tang, Jen-Yang ; Chang, Hsueh-Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c412t-6f3a31dcef9014d55f4dfba10bb9fcb06b1bbca7a0c17c13b908aebe739951193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Annexin V</topic><topic>Apoptosis</topic><topic>Cancer therapies</topic><topic>Cell Cycle</topic><topic>Cell growth</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cell viability</topic><topic>Chromones - chemistry</topic><topic>Chromones - pharmacology</topic><topic>Combined Modality Therapy</topic><topic>Cytotoxicity</topic><topic>Deoxyguanosine</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>Flow cytometry</topic><topic>Humans</topic><topic>Lung cancer</topic><topic>Membrane potential</topic><topic>Membrane Potential, Mitochondrial</topic><topic>Mitochondria</topic><topic>Mouth Neoplasms - drug therapy</topic><topic>Mouth Neoplasms - metabolism</topic><topic>Mouth Neoplasms - pathology</topic><topic>Mouth Neoplasms - radiotherapy</topic><topic>Oral cancer</topic><topic>Oxidative Stress</topic><topic>Poly (ADP-Ribose) Polymerase-1 - metabolism</topic><topic>Poly(ADP-ribose)</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Ribose</topic><topic>Tumor Cells, Cultured</topic><topic>Ultraviolet Rays</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Sheng-Chieh</creatorcontrib><creatorcontrib>Wang, Yen-Yun</creatorcontrib><creatorcontrib>Lin, Li-Ching</creatorcontrib><creatorcontrib>Chang, Meng-Yang</creatorcontrib><creatorcontrib>Yuan, Shyng-Shiou F</creatorcontrib><creatorcontrib>Tang, Jen-Yang</creatorcontrib><creatorcontrib>Chang, Hsueh-Wei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Sheng-Chieh</au><au>Wang, Yen-Yun</au><au>Lin, Li-Ching</au><au>Chang, Meng-Yang</au><au>Yuan, Shyng-Shiou F</au><au>Tang, Jen-Yang</au><au>Chang, Hsueh-Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Combined Treatment of Sulfonyl Chromen-4-Ones (CHW09) and Ultraviolet-C (UVC) Enhances Proliferation Inhibition, Apoptosis, Oxidative Stress, and DNA Damage against Oral Cancer Cells</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2020-09-03</date><risdate>2020</risdate><volume>21</volume><issue>17</issue><spage>6443</spage><pages>6443-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>The sensitizing effect of chromone-derived compounds on UVC-induced proliferation inhibition has not been comprehensively investigated so far. The subject of this study was to examine the proliferation change of oral cancer cells while using the combined treatment of UVC (254 nm) with our previously developed sulfonyl chromen-4-ones (CHW09), namely UVC/CHW09. Cell viability, apoptosis, oxidative stress, and DNA damage for the individual and combined treatments for UVC and/or CHW09 were examined in oral cancer Ca9-22 cells. In 24 h MTS assay, UVC (30 J/m
; UVC30), or CHW09 (25 and 50 µg/mL; namely, CHW09-25 and CHW09-50) show 54%, 59%, and 45% viability. The combined treatment (UVC30/CHW09-25 and UVC30/CHW09-50) show lower cell viability (45% and 35%). Mechanistically, UVC/CHW09 induced higher apoptosis than individual treatments and untreated control, which were supported by the evidence of flow cytometry for subG1, annexin V/7-aminoactinomycin D, pancaspase and caspases 3/7 activity, and western blotting for cleaved poly(ADP-ribose) polymerase. Moreover, this cleaved PARP expression was downregulated by pancaspase inhibitor Z-VAD-FMK. UVC/CHW09 showed higher oxidative stress than individual treatments and untreated control in terms of flow cytometry for reactive oxygen species, mitochondrial membrane potential, and mitochondrial mass. Furthermore, UVC/CHW09 showed higher DNA damage than individual treatments and untreated control in terms of flow cytometry for H2A histone family member X and 8-oxo-2'-deoxyguanosine. In conclusion, combined treatment UVC/CHW09 suppresses proliferation, and promotes apoptosis, oxidative stress, and DNA damage against oral cancer cells, providing a novel application of sulfonyl chromen-4-ones in order to sensitize UVC induced proliferation inhibition for oral cancer therapy.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>32899415</pmid><doi>10.3390/ijms21176443</doi><orcidid>https://orcid.org/0000-0002-1983-8570</orcidid><orcidid>https://orcid.org/0000-0002-4753-788X</orcidid><orcidid>https://orcid.org/0000-0003-0068-2366</orcidid><orcidid>https://orcid.org/0000-0002-5690-0708</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Annexin V Apoptosis Cancer therapies Cell Cycle Cell growth Cell Movement Cell Proliferation Cell viability Chromones - chemistry Chromones - pharmacology Combined Modality Therapy Cytotoxicity Deoxyguanosine Deoxyribonucleic acid DNA DNA Damage Flow cytometry Humans Lung cancer Membrane potential Membrane Potential, Mitochondrial Mitochondria Mouth Neoplasms - drug therapy Mouth Neoplasms - metabolism Mouth Neoplasms - pathology Mouth Neoplasms - radiotherapy Oral cancer Oxidative Stress Poly (ADP-Ribose) Polymerase-1 - metabolism Poly(ADP-ribose) Poly(ADP-ribose) polymerase Reactive oxygen species Reactive Oxygen Species - metabolism Ribose Tumor Cells, Cultured Ultraviolet Rays Western blotting |
| title | Combined Treatment of Sulfonyl Chromen-4-Ones (CHW09) and Ultraviolet-C (UVC) Enhances Proliferation Inhibition, Apoptosis, Oxidative Stress, and DNA Damage against Oral Cancer Cells |
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