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Isoliquiritigenin as a cause of DNA damage and inhibitor of ataxia-telangiectasia mutated expression leading to G2/M phase arrest and apoptosis in oral squamous cell carcinoma
Background Isoliquiritigenin (ISL), a natural compound extracted from licorice, has chemopreventive and antitumor activities. The purpose of this study was to investigate the anticancer effect of ISL on human oral squamous cell carcinoma (OSCC). Methods The anti‐OSCC effects of ISL were evaluated us...
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| Published in: | Head & neck 2016-04, Vol.38 (S1), p.E360-E371 |
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| container_end_page | E371 |
| container_issue | S1 |
| container_start_page | E360 |
| container_title | Head & neck |
| container_volume | 38 |
| creator | Hsia, Shih-Min Yu, Cheng-Chia Shih, Yin-Hua Yuanchien Chen, Michael Wang, Tong-Hong Huang, Yu-Ting Shieh, Tzong-Ming |
| description | Background
Isoliquiritigenin (ISL), a natural compound extracted from licorice, has chemopreventive and antitumor activities. The purpose of this study was to investigate the anticancer effect of ISL on human oral squamous cell carcinoma (OSCC).
Methods
The anti‐OSCC effects of ISL were evaluated using the 3‐(4,5‐dimethylthiazol‐2‐yl)−2,5‐diphenyltetrazolium bromide test, flow cytometry, reverse transcription‐polymerase chain reaction, Western blotting, promoter activity, terminal deoxynucleotidyl transferase dUTP nick‐end labeling assay, malignant phenotype analysis, microRNA, and xenografting.
Results
ISL induced OSCC cell cycle G2/M phase arrest, apoptosis, and DNA damage. However, the DNA repair‐associated ataxia telangiectasia mutated (ATM) and phospho‐ATM were downregulated, ATM mRNA remained unchanged, and the downstream signals were inhibited. ATM recovered when the caspase activity was blocked by Z‐DVED‐FMK. A low dose of ISL inhibited OSCC malignancy in vitro and reduced the tumor size in vivo.
Conclusion
ATM was cleaved by ISL‐activated caspase, thus inhibiting DNA repair in OSCC cells. Therefore, ISL is a promising chemopreventive agent against oral cancer. © 2015 Wiley Periodicals, Inc. Head Neck 38: E360–E371, 2016 |
| doi_str_mv | 10.1002/hed.24001 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1794501453</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1784744996</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3961-b635c2f7efef0d22c61640bc794cc169f0d6cb6de97e3c3d613b8422fe8604553</originalsourceid><addsrcrecordid>eNqNkc9u1DAQhyMEoqVw4AWQj3BI1__iJMeqLduKUoQEVOJiTZzJriGJs7Yjtk_FK-LtdrkhcbI1883nsX5Z9prRU0YpX6yxPeWSUvYkO2a0LnMqZPl0d5ciF7SUR9mLEH5QSoWS_Hl2xIuiokWljrPf18H1djNbb6Nd4WhHAoEAMTAHJK4jF7dnpIUBVkhgbIkd17ax0fldDyJsLeQRexhXFk2EYIEMc4SILcHt5DEE60bSI7R2XJHoyJIvPpJpDckOPvXjgxYmN0UXbEgPEOehJ2Ezw-DmQAz2fVrHGzu6AV5mzzroA756PE-yr-8vv5xf5TefltfnZze5EbVieaNEYXhXYocdbTk3iilJG1PW0him6lRUplEt1iUKI1rFRFNJzjusFJVFIU6yt3vv5N1mTmvqwYbdKjBi2kqzZCook4X4D7SSpZR1rRL6bo8a70Lw2OnJ2wH8vWZU76LUKUr9EGVi3zxq52ZI1QN5yC4Biz3wy_Z4_2-Tvrq8OCjz_YQNEbd_J8D_1KoUZaHvbpf6W5W-9uH7nf4s_gBajbmJ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1784744996</pqid></control><display><type>article</type><title>Isoliquiritigenin as a cause of DNA damage and inhibitor of ataxia-telangiectasia mutated expression leading to G2/M phase arrest and apoptosis in oral squamous cell carcinoma</title><source>Wiley-Blackwell Read & Publish Collection</source><creator>Hsia, Shih-Min ; Yu, Cheng-Chia ; Shih, Yin-Hua ; Yuanchien Chen, Michael ; Wang, Tong-Hong ; Huang, Yu-Ting ; Shieh, Tzong-Ming</creator><creatorcontrib>Hsia, Shih-Min ; Yu, Cheng-Chia ; Shih, Yin-Hua ; Yuanchien Chen, Michael ; Wang, Tong-Hong ; Huang, Yu-Ting ; Shieh, Tzong-Ming</creatorcontrib><description>Background
Isoliquiritigenin (ISL), a natural compound extracted from licorice, has chemopreventive and antitumor activities. The purpose of this study was to investigate the anticancer effect of ISL on human oral squamous cell carcinoma (OSCC).
Methods
The anti‐OSCC effects of ISL were evaluated using the 3‐(4,5‐dimethylthiazol‐2‐yl)−2,5‐diphenyltetrazolium bromide test, flow cytometry, reverse transcription‐polymerase chain reaction, Western blotting, promoter activity, terminal deoxynucleotidyl transferase dUTP nick‐end labeling assay, malignant phenotype analysis, microRNA, and xenografting.
Results
ISL induced OSCC cell cycle G2/M phase arrest, apoptosis, and DNA damage. However, the DNA repair‐associated ataxia telangiectasia mutated (ATM) and phospho‐ATM were downregulated, ATM mRNA remained unchanged, and the downstream signals were inhibited. ATM recovered when the caspase activity was blocked by Z‐DVED‐FMK. A low dose of ISL inhibited OSCC malignancy in vitro and reduced the tumor size in vivo.
Conclusion
ATM was cleaved by ISL‐activated caspase, thus inhibiting DNA repair in OSCC cells. Therefore, ISL is a promising chemopreventive agent against oral cancer. © 2015 Wiley Periodicals, Inc. Head Neck 38: E360–E371, 2016</description><identifier>ISSN: 1043-3074</identifier><identifier>EISSN: 1097-0347</identifier><identifier>DOI: 10.1002/hed.24001</identifier><identifier>PMID: 25580586</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>Apoptosis ; ataxia telangiectasia mutated (ATM) ; Ataxia Telangiectasia Mutated Proteins - genetics ; Ataxia Telangiectasia Mutated Proteins - metabolism ; Carcinoma, Squamous Cell - drug therapy ; Carcinoma, Squamous Cell - pathology ; Cell Cycle Checkpoints - drug effects ; Cell Division ; Cell Line, Tumor ; Chalcones - pharmacology ; DNA Damage ; Glycyrrhiza glabra ; Humans ; isoliquiritigenin ; Mouth Neoplasms - drug therapy ; Mouth Neoplasms - pathology ; oral squamous cell carcinoma (OSCC)</subject><ispartof>Head & neck, 2016-04, Vol.38 (S1), p.E360-E371</ispartof><rights>2015 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3961-b635c2f7efef0d22c61640bc794cc169f0d6cb6de97e3c3d613b8422fe8604553</citedby><cites>FETCH-LOGICAL-c3961-b635c2f7efef0d22c61640bc794cc169f0d6cb6de97e3c3d613b8422fe8604553</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25580586$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hsia, Shih-Min</creatorcontrib><creatorcontrib>Yu, Cheng-Chia</creatorcontrib><creatorcontrib>Shih, Yin-Hua</creatorcontrib><creatorcontrib>Yuanchien Chen, Michael</creatorcontrib><creatorcontrib>Wang, Tong-Hong</creatorcontrib><creatorcontrib>Huang, Yu-Ting</creatorcontrib><creatorcontrib>Shieh, Tzong-Ming</creatorcontrib><title>Isoliquiritigenin as a cause of DNA damage and inhibitor of ataxia-telangiectasia mutated expression leading to G2/M phase arrest and apoptosis in oral squamous cell carcinoma</title><title>Head & neck</title><addtitle>Head Neck</addtitle><description>Background
Isoliquiritigenin (ISL), a natural compound extracted from licorice, has chemopreventive and antitumor activities. The purpose of this study was to investigate the anticancer effect of ISL on human oral squamous cell carcinoma (OSCC).
Methods
The anti‐OSCC effects of ISL were evaluated using the 3‐(4,5‐dimethylthiazol‐2‐yl)−2,5‐diphenyltetrazolium bromide test, flow cytometry, reverse transcription‐polymerase chain reaction, Western blotting, promoter activity, terminal deoxynucleotidyl transferase dUTP nick‐end labeling assay, malignant phenotype analysis, microRNA, and xenografting.
Results
ISL induced OSCC cell cycle G2/M phase arrest, apoptosis, and DNA damage. However, the DNA repair‐associated ataxia telangiectasia mutated (ATM) and phospho‐ATM were downregulated, ATM mRNA remained unchanged, and the downstream signals were inhibited. ATM recovered when the caspase activity was blocked by Z‐DVED‐FMK. A low dose of ISL inhibited OSCC malignancy in vitro and reduced the tumor size in vivo.
Conclusion
ATM was cleaved by ISL‐activated caspase, thus inhibiting DNA repair in OSCC cells. Therefore, ISL is a promising chemopreventive agent against oral cancer. © 2015 Wiley Periodicals, Inc. Head Neck 38: E360–E371, 2016</description><subject>Apoptosis</subject><subject>ataxia telangiectasia mutated (ATM)</subject><subject>Ataxia Telangiectasia Mutated Proteins - genetics</subject><subject>Ataxia Telangiectasia Mutated Proteins - metabolism</subject><subject>Carcinoma, Squamous Cell - drug therapy</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell Cycle Checkpoints - drug effects</subject><subject>Cell Division</subject><subject>Cell Line, Tumor</subject><subject>Chalcones - pharmacology</subject><subject>DNA Damage</subject><subject>Glycyrrhiza glabra</subject><subject>Humans</subject><subject>isoliquiritigenin</subject><subject>Mouth Neoplasms - drug therapy</subject><subject>Mouth Neoplasms - pathology</subject><subject>oral squamous cell carcinoma (OSCC)</subject><issn>1043-3074</issn><issn>1097-0347</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNqNkc9u1DAQhyMEoqVw4AWQj3BI1__iJMeqLduKUoQEVOJiTZzJriGJs7Yjtk_FK-LtdrkhcbI1883nsX5Z9prRU0YpX6yxPeWSUvYkO2a0LnMqZPl0d5ciF7SUR9mLEH5QSoWS_Hl2xIuiokWljrPf18H1djNbb6Nd4WhHAoEAMTAHJK4jF7dnpIUBVkhgbIkd17ax0fldDyJsLeQRexhXFk2EYIEMc4SILcHt5DEE60bSI7R2XJHoyJIvPpJpDckOPvXjgxYmN0UXbEgPEOehJ2Ezw-DmQAz2fVrHGzu6AV5mzzroA756PE-yr-8vv5xf5TefltfnZze5EbVieaNEYXhXYocdbTk3iilJG1PW0him6lRUplEt1iUKI1rFRFNJzjusFJVFIU6yt3vv5N1mTmvqwYbdKjBi2kqzZCook4X4D7SSpZR1rRL6bo8a70Lw2OnJ2wH8vWZU76LUKUr9EGVi3zxq52ZI1QN5yC4Biz3wy_Z4_2-Tvrq8OCjz_YQNEbd_J8D_1KoUZaHvbpf6W5W-9uH7nf4s_gBajbmJ</recordid><startdate>201604</startdate><enddate>201604</enddate><creator>Hsia, Shih-Min</creator><creator>Yu, Cheng-Chia</creator><creator>Shih, Yin-Hua</creator><creator>Yuanchien Chen, Michael</creator><creator>Wang, Tong-Hong</creator><creator>Huang, Yu-Ting</creator><creator>Shieh, Tzong-Ming</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><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>7X8</scope><scope>7TK</scope><scope>7TM</scope></search><sort><creationdate>201604</creationdate><title>Isoliquiritigenin as a cause of DNA damage and inhibitor of ataxia-telangiectasia mutated expression leading to G2/M phase arrest and apoptosis in oral squamous cell carcinoma</title><author>Hsia, Shih-Min ; Yu, Cheng-Chia ; Shih, Yin-Hua ; Yuanchien Chen, Michael ; Wang, Tong-Hong ; Huang, Yu-Ting ; Shieh, Tzong-Ming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3961-b635c2f7efef0d22c61640bc794cc169f0d6cb6de97e3c3d613b8422fe8604553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Apoptosis</topic><topic>ataxia telangiectasia mutated (ATM)</topic><topic>Ataxia Telangiectasia Mutated Proteins - genetics</topic><topic>Ataxia Telangiectasia Mutated Proteins - metabolism</topic><topic>Carcinoma, Squamous Cell - drug therapy</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell Cycle Checkpoints - drug effects</topic><topic>Cell Division</topic><topic>Cell Line, Tumor</topic><topic>Chalcones - pharmacology</topic><topic>DNA Damage</topic><topic>Glycyrrhiza glabra</topic><topic>Humans</topic><topic>isoliquiritigenin</topic><topic>Mouth Neoplasms - drug therapy</topic><topic>Mouth Neoplasms - pathology</topic><topic>oral squamous cell carcinoma (OSCC)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hsia, Shih-Min</creatorcontrib><creatorcontrib>Yu, Cheng-Chia</creatorcontrib><creatorcontrib>Shih, Yin-Hua</creatorcontrib><creatorcontrib>Yuanchien Chen, Michael</creatorcontrib><creatorcontrib>Wang, Tong-Hong</creatorcontrib><creatorcontrib>Huang, Yu-Ting</creatorcontrib><creatorcontrib>Shieh, Tzong-Ming</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><jtitle>Head & neck</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hsia, Shih-Min</au><au>Yu, Cheng-Chia</au><au>Shih, Yin-Hua</au><au>Yuanchien Chen, Michael</au><au>Wang, Tong-Hong</au><au>Huang, Yu-Ting</au><au>Shieh, Tzong-Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Isoliquiritigenin as a cause of DNA damage and inhibitor of ataxia-telangiectasia mutated expression leading to G2/M phase arrest and apoptosis in oral squamous cell carcinoma</atitle><jtitle>Head & neck</jtitle><addtitle>Head Neck</addtitle><date>2016-04</date><risdate>2016</risdate><volume>38</volume><issue>S1</issue><spage>E360</spage><epage>E371</epage><pages>E360-E371</pages><issn>1043-3074</issn><eissn>1097-0347</eissn><abstract>Background
Isoliquiritigenin (ISL), a natural compound extracted from licorice, has chemopreventive and antitumor activities. The purpose of this study was to investigate the anticancer effect of ISL on human oral squamous cell carcinoma (OSCC).
Methods
The anti‐OSCC effects of ISL were evaluated using the 3‐(4,5‐dimethylthiazol‐2‐yl)−2,5‐diphenyltetrazolium bromide test, flow cytometry, reverse transcription‐polymerase chain reaction, Western blotting, promoter activity, terminal deoxynucleotidyl transferase dUTP nick‐end labeling assay, malignant phenotype analysis, microRNA, and xenografting.
Results
ISL induced OSCC cell cycle G2/M phase arrest, apoptosis, and DNA damage. However, the DNA repair‐associated ataxia telangiectasia mutated (ATM) and phospho‐ATM were downregulated, ATM mRNA remained unchanged, and the downstream signals were inhibited. ATM recovered when the caspase activity was blocked by Z‐DVED‐FMK. A low dose of ISL inhibited OSCC malignancy in vitro and reduced the tumor size in vivo.
Conclusion
ATM was cleaved by ISL‐activated caspase, thus inhibiting DNA repair in OSCC cells. Therefore, ISL is a promising chemopreventive agent against oral cancer. © 2015 Wiley Periodicals, Inc. Head Neck 38: E360–E371, 2016</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>25580586</pmid><doi>10.1002/hed.24001</doi><tpages>12</tpages></addata></record> |
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| subjects | Apoptosis ataxia telangiectasia mutated (ATM) Ataxia Telangiectasia Mutated Proteins - genetics Ataxia Telangiectasia Mutated Proteins - metabolism Carcinoma, Squamous Cell - drug therapy Carcinoma, Squamous Cell - pathology Cell Cycle Checkpoints - drug effects Cell Division Cell Line, Tumor Chalcones - pharmacology DNA Damage Glycyrrhiza glabra Humans isoliquiritigenin Mouth Neoplasms - drug therapy Mouth Neoplasms - pathology oral squamous cell carcinoma (OSCC) |
| title | Isoliquiritigenin as a cause of DNA damage and inhibitor of ataxia-telangiectasia mutated expression leading to G2/M phase arrest and apoptosis in oral squamous cell carcinoma |
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