Epigallocatechin gallate sensitizes cisplatin‐resistant oral cancer CAR cell apoptosis and autophagy through stimulating AKT/STAT3 pathway and suppressing multidrug resistance 1 signaling
Epigallocatechin gallate (EGCG) is a green tea polyphenol that presents anticancer activities in multiple cancer cells, but no available report was addressed for the underling molecular mechanism of cytotoxic impacts on drug‐resistant oral squamous cell carcinoma cells. In the present study, the inh...
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| Veröffentlicht in: | Environmental toxicology 2017-03, Vol.32 (3), p.845-855 |
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| creator | Yuan, Chien‐Han Horng, Chi‐Ting Lee, Chiu‐Fang Chiang, Ni‐Na Tsai, Fuu‐Jen Lu, Chi‐Cheng Chiang, Jo‐Hua Hsu, Yuan‐Man Yang, Jai‐Sing Chen, Fu‐An |
| description | Epigallocatechin gallate (EGCG) is a green tea polyphenol that presents anticancer activities in multiple cancer cells, but no available report was addressed for the underling molecular mechanism of cytotoxic impacts on drug‐resistant oral squamous cell carcinoma cells. In the present study, the inhibitory effects of EGCG were experienced on cisplatin‐resistant oral cancer CAR cells. EGCG inhibited cell viability in a time‐ and concentration‐dependent manner by a sulforhodamine B (SRB) assay. EGCG induced CAR cell apoptosis and autophagy by 4′,6‐diamidino‐2‐phenylindole (DAPI) dye, acridine orange (AO) staining and green fluorescent protein (GFP)‐tagged LC3B assay, respectively. EGCG also significantly enhanced caspase‐9 and caspase‐3 activities by caspase activity assay. EGCG markedly increased the protein levels of Bax, cleaved caspase‐9, cleaved caspase‐3, Atg5, Atg7, Atg12, Beclin‐1, and LC3B‐II, as well as significantly decreased the expression of Bcl‐2, phosphorylated AKT (Ser473) and phosphorylation of STAT3 on Tyr705 by western blotting in CAR cells. Importantly, the protein and gene expression of multidrug resistance 1 (MDR1) were dose‐dependently inhibited by EGCG. Overall, downregulation of MDR1 levels and alterations of AKT/STAT3 signaling contributed to EGCG‐induced apoptosis and autophagy in CAR cells. Based on these results, EGCG has the potential for therapeutic effect on oral cancer and may be useful for long‐term oral cancer prevention in the future. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 845–855, 2017. |
| doi_str_mv | 10.1002/tox.22284 |
| format | Article |
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In the present study, the inhibitory effects of EGCG were experienced on cisplatin‐resistant oral cancer CAR cells. EGCG inhibited cell viability in a time‐ and concentration‐dependent manner by a sulforhodamine B (SRB) assay. EGCG induced CAR cell apoptosis and autophagy by 4′,6‐diamidino‐2‐phenylindole (DAPI) dye, acridine orange (AO) staining and green fluorescent protein (GFP)‐tagged LC3B assay, respectively. EGCG also significantly enhanced caspase‐9 and caspase‐3 activities by caspase activity assay. EGCG markedly increased the protein levels of Bax, cleaved caspase‐9, cleaved caspase‐3, Atg5, Atg7, Atg12, Beclin‐1, and LC3B‐II, as well as significantly decreased the expression of Bcl‐2, phosphorylated AKT (Ser473) and phosphorylation of STAT3 on Tyr705 by western blotting in CAR cells. Importantly, the protein and gene expression of multidrug resistance 1 (MDR1) were dose‐dependently inhibited by EGCG. Overall, downregulation of MDR1 levels and alterations of AKT/STAT3 signaling contributed to EGCG‐induced apoptosis and autophagy in CAR cells. Based on these results, EGCG has the potential for therapeutic effect on oral cancer and may be useful for long‐term oral cancer prevention in the future. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 845–855, 2017.</description><identifier>ISSN: 1520-4081</identifier><identifier>EISSN: 1522-7278</identifier><identifier>DOI: 10.1002/tox.22284</identifier><identifier>PMID: 27200496</identifier><identifier>CODEN: ETOXFH</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>AKT/STAT3 signaling ; apoptosis ; Apoptosis - drug effects ; Apoptosis Regulatory Proteins - metabolism ; ATP-Binding Cassette, Sub-Family B, Member 1 - genetics ; ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism ; autophagy ; Autophagy - drug effects ; Autophagy-Related Proteins - metabolism ; Caspase 3 - metabolism ; Caspase 9 - metabolism ; Catechin - analogs & derivatives ; Catechin - pharmacology ; Cell Line, Tumor ; Cisplatin - pharmacology ; Cisplatin - toxicity ; Down-Regulation - drug effects ; epigallocatechin gallate ; Humans ; MDR1 ; Microscopy, Fluorescence ; Mouth Neoplasms - metabolism ; Mouth Neoplasms - pathology ; Phosphorylation - drug effects ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction - drug effects ; STAT3 Transcription Factor - metabolism</subject><ispartof>Environmental toxicology, 2017-03, Vol.32 (3), p.845-855</ispartof><rights>2016 Wiley Periodicals, Inc.</rights><rights>2017 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3894-e35bea58814f2051005617dcc0e650f5b7e33efee4d8fbc35e30c545dc50868e3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Ftox.22284$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Ftox.22284$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27200496$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yuan, Chien‐Han</creatorcontrib><creatorcontrib>Horng, Chi‐Ting</creatorcontrib><creatorcontrib>Lee, Chiu‐Fang</creatorcontrib><creatorcontrib>Chiang, Ni‐Na</creatorcontrib><creatorcontrib>Tsai, Fuu‐Jen</creatorcontrib><creatorcontrib>Lu, Chi‐Cheng</creatorcontrib><creatorcontrib>Chiang, Jo‐Hua</creatorcontrib><creatorcontrib>Hsu, Yuan‐Man</creatorcontrib><creatorcontrib>Yang, Jai‐Sing</creatorcontrib><creatorcontrib>Chen, Fu‐An</creatorcontrib><title>Epigallocatechin gallate sensitizes cisplatin‐resistant oral cancer CAR cell apoptosis and autophagy through stimulating AKT/STAT3 pathway and suppressing multidrug resistance 1 signaling</title><title>Environmental toxicology</title><addtitle>Environ Toxicol</addtitle><description>Epigallocatechin gallate (EGCG) is a green tea polyphenol that presents anticancer activities in multiple cancer cells, but no available report was addressed for the underling molecular mechanism of cytotoxic impacts on drug‐resistant oral squamous cell carcinoma cells. In the present study, the inhibitory effects of EGCG were experienced on cisplatin‐resistant oral cancer CAR cells. EGCG inhibited cell viability in a time‐ and concentration‐dependent manner by a sulforhodamine B (SRB) assay. EGCG induced CAR cell apoptosis and autophagy by 4′,6‐diamidino‐2‐phenylindole (DAPI) dye, acridine orange (AO) staining and green fluorescent protein (GFP)‐tagged LC3B assay, respectively. EGCG also significantly enhanced caspase‐9 and caspase‐3 activities by caspase activity assay. EGCG markedly increased the protein levels of Bax, cleaved caspase‐9, cleaved caspase‐3, Atg5, Atg7, Atg12, Beclin‐1, and LC3B‐II, as well as significantly decreased the expression of Bcl‐2, phosphorylated AKT (Ser473) and phosphorylation of STAT3 on Tyr705 by western blotting in CAR cells. Importantly, the protein and gene expression of multidrug resistance 1 (MDR1) were dose‐dependently inhibited by EGCG. Overall, downregulation of MDR1 levels and alterations of AKT/STAT3 signaling contributed to EGCG‐induced apoptosis and autophagy in CAR cells. Based on these results, EGCG has the potential for therapeutic effect on oral cancer and may be useful for long‐term oral cancer prevention in the future. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 845–855, 2017.</description><subject>AKT/STAT3 signaling</subject><subject>apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>ATP-Binding Cassette, Sub-Family B, Member 1 - genetics</subject><subject>ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism</subject><subject>autophagy</subject><subject>Autophagy - drug effects</subject><subject>Autophagy-Related Proteins - metabolism</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase 9 - metabolism</subject><subject>Catechin - analogs & derivatives</subject><subject>Catechin - pharmacology</subject><subject>Cell Line, Tumor</subject><subject>Cisplatin - pharmacology</subject><subject>Cisplatin - toxicity</subject><subject>Down-Regulation - drug effects</subject><subject>epigallocatechin gallate</subject><subject>Humans</subject><subject>MDR1</subject><subject>Microscopy, Fluorescence</subject><subject>Mouth Neoplasms - metabolism</subject><subject>Mouth Neoplasms - pathology</subject><subject>Phosphorylation - drug effects</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>STAT3 Transcription Factor - metabolism</subject><issn>1520-4081</issn><issn>1522-7278</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1u1DAUhS1ERUthwQsgS2zYpOOfOPEsR6NSKipVKkFiF3mcm8RVJjaxrTKs-gi8EC_TJ8FJWxasfHz9-R77HoTeUXJGCWGrYH-eMcZk_gKdUMFYVrJSvlw0yXIi6TF67f0tIWRdiOIVOmYlIyRfFyfoz7kznRoGq1UA3ZsRz7uksYfRm2B-gcfaeJdqZny4_z2BNz6oMWA7qQFrNWqY8HZzgzUMA1bOumATgtXYYBWDdb3qDjj0k41dj30w-7j06vDmS7X6Wm0qjp0K_Z06LHd8dC6Z-JlIaDDNFDv8bKsBU-xNN6ohAW_QUasGD2-f1lP07dN5tf2cXV1fXG43V5nmcp1nwMUOlJCS5i0jIs1MFLRstCZQCNKKXQmcQwuQN7LdaS6AEy1y0WhBZCGBn6KPj33dZH9E8KHeGz__V41go6-pLNP0SXJI6If_0Fsbp_TcmSokpUWKIVHvn6i420NTu8ns1XSon4NJwOoRuDMDHP6dU1LPidcp8XpJvK6uvy-C_wWSv6MS</recordid><startdate>201703</startdate><enddate>201703</enddate><creator>Yuan, Chien‐Han</creator><creator>Horng, Chi‐Ting</creator><creator>Lee, Chiu‐Fang</creator><creator>Chiang, Ni‐Na</creator><creator>Tsai, Fuu‐Jen</creator><creator>Lu, Chi‐Cheng</creator><creator>Chiang, Jo‐Hua</creator><creator>Hsu, Yuan‐Man</creator><creator>Yang, Jai‐Sing</creator><creator>Chen, Fu‐An</creator><general>Wiley Subscription Services, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QH</scope><scope>7ST</scope><scope>7TN</scope><scope>7U7</scope><scope>7UA</scope><scope>C1K</scope><scope>F1W</scope><scope>H97</scope><scope>K9.</scope><scope>L.G</scope><scope>M7N</scope><scope>SOI</scope></search><sort><creationdate>201703</creationdate><title>Epigallocatechin gallate sensitizes cisplatin‐resistant oral cancer CAR cell apoptosis and autophagy through stimulating AKT/STAT3 pathway and suppressing multidrug resistance 1 signaling</title><author>Yuan, Chien‐Han ; Horng, Chi‐Ting ; Lee, Chiu‐Fang ; Chiang, Ni‐Na ; Tsai, Fuu‐Jen ; Lu, Chi‐Cheng ; Chiang, Jo‐Hua ; Hsu, Yuan‐Man ; Yang, Jai‐Sing ; Chen, Fu‐An</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3894-e35bea58814f2051005617dcc0e650f5b7e33efee4d8fbc35e30c545dc50868e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>AKT/STAT3 signaling</topic><topic>apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>ATP-Binding Cassette, Sub-Family B, Member 1 - genetics</topic><topic>ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism</topic><topic>autophagy</topic><topic>Autophagy - drug effects</topic><topic>Autophagy-Related Proteins - metabolism</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase 9 - metabolism</topic><topic>Catechin - analogs & derivatives</topic><topic>Catechin - pharmacology</topic><topic>Cell Line, Tumor</topic><topic>Cisplatin - pharmacology</topic><topic>Cisplatin - toxicity</topic><topic>Down-Regulation - drug effects</topic><topic>epigallocatechin gallate</topic><topic>Humans</topic><topic>MDR1</topic><topic>Microscopy, Fluorescence</topic><topic>Mouth Neoplasms - metabolism</topic><topic>Mouth Neoplasms - pathology</topic><topic>Phosphorylation - drug effects</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>STAT3 Transcription Factor - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yuan, Chien‐Han</creatorcontrib><creatorcontrib>Horng, Chi‐Ting</creatorcontrib><creatorcontrib>Lee, Chiu‐Fang</creatorcontrib><creatorcontrib>Chiang, Ni‐Na</creatorcontrib><creatorcontrib>Tsai, Fuu‐Jen</creatorcontrib><creatorcontrib>Lu, Chi‐Cheng</creatorcontrib><creatorcontrib>Chiang, Jo‐Hua</creatorcontrib><creatorcontrib>Hsu, Yuan‐Man</creatorcontrib><creatorcontrib>Yang, Jai‐Sing</creatorcontrib><creatorcontrib>Chen, Fu‐An</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Aqualine</collection><collection>Environment Abstracts</collection><collection>Oceanic Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Water Resources Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Environment Abstracts</collection><jtitle>Environmental toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yuan, Chien‐Han</au><au>Horng, Chi‐Ting</au><au>Lee, Chiu‐Fang</au><au>Chiang, Ni‐Na</au><au>Tsai, Fuu‐Jen</au><au>Lu, Chi‐Cheng</au><au>Chiang, Jo‐Hua</au><au>Hsu, Yuan‐Man</au><au>Yang, Jai‐Sing</au><au>Chen, Fu‐An</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epigallocatechin gallate sensitizes cisplatin‐resistant oral cancer CAR cell apoptosis and autophagy through stimulating AKT/STAT3 pathway and suppressing multidrug resistance 1 signaling</atitle><jtitle>Environmental toxicology</jtitle><addtitle>Environ Toxicol</addtitle><date>2017-03</date><risdate>2017</risdate><volume>32</volume><issue>3</issue><spage>845</spage><epage>855</epage><pages>845-855</pages><issn>1520-4081</issn><eissn>1522-7278</eissn><coden>ETOXFH</coden><abstract>Epigallocatechin gallate (EGCG) is a green tea polyphenol that presents anticancer activities in multiple cancer cells, but no available report was addressed for the underling molecular mechanism of cytotoxic impacts on drug‐resistant oral squamous cell carcinoma cells. In the present study, the inhibitory effects of EGCG were experienced on cisplatin‐resistant oral cancer CAR cells. EGCG inhibited cell viability in a time‐ and concentration‐dependent manner by a sulforhodamine B (SRB) assay. EGCG induced CAR cell apoptosis and autophagy by 4′,6‐diamidino‐2‐phenylindole (DAPI) dye, acridine orange (AO) staining and green fluorescent protein (GFP)‐tagged LC3B assay, respectively. EGCG also significantly enhanced caspase‐9 and caspase‐3 activities by caspase activity assay. EGCG markedly increased the protein levels of Bax, cleaved caspase‐9, cleaved caspase‐3, Atg5, Atg7, Atg12, Beclin‐1, and LC3B‐II, as well as significantly decreased the expression of Bcl‐2, phosphorylated AKT (Ser473) and phosphorylation of STAT3 on Tyr705 by western blotting in CAR cells. Importantly, the protein and gene expression of multidrug resistance 1 (MDR1) were dose‐dependently inhibited by EGCG. Overall, downregulation of MDR1 levels and alterations of AKT/STAT3 signaling contributed to EGCG‐induced apoptosis and autophagy in CAR cells. Based on these results, EGCG has the potential for therapeutic effect on oral cancer and may be useful for long‐term oral cancer prevention in the future. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 845–855, 2017.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>27200496</pmid><doi>10.1002/tox.22284</doi><tpages>11</tpages></addata></record> |
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| subjects | AKT/STAT3 signaling apoptosis Apoptosis - drug effects Apoptosis Regulatory Proteins - metabolism ATP-Binding Cassette, Sub-Family B, Member 1 - genetics ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism autophagy Autophagy - drug effects Autophagy-Related Proteins - metabolism Caspase 3 - metabolism Caspase 9 - metabolism Catechin - analogs & derivatives Catechin - pharmacology Cell Line, Tumor Cisplatin - pharmacology Cisplatin - toxicity Down-Regulation - drug effects epigallocatechin gallate Humans MDR1 Microscopy, Fluorescence Mouth Neoplasms - metabolism Mouth Neoplasms - pathology Phosphorylation - drug effects Proto-Oncogene Proteins c-akt - metabolism Signal Transduction - drug effects STAT3 Transcription Factor - metabolism |
| title | Epigallocatechin gallate sensitizes cisplatin‐resistant oral cancer CAR cell apoptosis and autophagy through stimulating AKT/STAT3 pathway and suppressing multidrug resistance 1 signaling |
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