Tannic acid inhibits the Jak2/STAT3 pathway and induces G1/S arrest and mitochondrial apoptosis in YD-38 gingival cancer cells
Tannic acid (TA), is a potent anti-oxidant, showing anti-proliferative effects on numerous cancers. The ability of TA to induce proliferation inhibition on the rare tumor, gingival squamous cell carcinoma (GSCC), comprising
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| Veröffentlicht in: | International journal of oncology 2015-09, Vol.47 (3), p.1111-1120 |
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| container_title | International journal of oncology |
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| creator | DARVIN, PRAMOD BAEG, SEUNG JO JOUNG, YOUN HEE SP, NIPIN KANG, DONG YOUNG BYUN, HYO JOO PARK, JE UK YANG, YOUNG MOK |
| description | Tannic acid (TA), is a potent anti-oxidant, showing anti-proliferative effects on numerous cancers. The ability of TA to induce proliferation inhibition on the rare tumor, gingival squamous cell carcinoma (GSCC), comprising |
| doi_str_mv | 10.3892/ijo.2015.3098 |
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The ability of TA to induce proliferation inhibition on the rare tumor, gingival squamous cell carcinoma (GSCC), comprising <10% of all head and neck squamous cell carcinomas was studied in the YD-38 cell line. The main goal was to modulate the Jak2/STAT3 pathway using TA and to induce cell cycle arrest and apoptosis in GSCC. TA treatment induced G1 arrest and apoptosis in YD-38 cells. Molecular analysis revealed that TA inhibits Jak2/STAT3 pathway by preventing their expression as well as phosphorylation. This inhibition of STAT3 phosphorylation prevented the nuclear translocation and DNA binding capability of STAT3. Together with the inhibition of transcriptional regulatory function of STAT3, TA inhibited the expression of G1 phase modulators CDK-4, CDK-6, cyclin D1 and cyclin E. It is also evidenced that TA exerted an intense activation of p21Waf1/Cip1, p27Kip1 and p53 genes confirming its role in G1 phase inhibition. Additionally, upon treatment with TA, the expression of mitochondrial pore factors Bax, Bcl-2 and Bcl-XL were changed. We observed inhibition of Bcl-2 and an increase in mitochondrial localization of Bax leading to the loss of mitochondrial membrane potential, resulting in the release of cytochrome c to the cytosol. In addition, we perceived the activation of caspases upon TA treatment. Specific inhibition of caspase protected the cells from TA induced apoptosis. Taken together, this study reveals that TA significantly inhibits the Jak2/STAT3 signaling pathway and induces G1 arrest and mitochondrial apoptosis in YD-38 cells.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2015.3098</identifier><identifier>PMID: 26202061</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Analysis ; Antineoplastic Agents - pharmacology ; Apoptosis ; Cancer ; Carcinoma, Squamous Cell - drug therapy ; Carcinoma, Squamous Cell - metabolism ; Cell cycle ; Cell Cycle - drug effects ; Cell growth ; Cell Line, Tumor ; Cytochrome ; Drug therapy ; G1 arrest ; Gene Expression Regulation, Neoplastic - drug effects ; Genetic aspects ; Gingival Neoplasms - drug therapy ; Gingival Neoplasms - metabolism ; Health aspects ; Humans ; Immunoglobulins ; intrinsic apoptosis ; Jak2/STAT3 ; Janus Kinase 2 - metabolism ; Kinases ; Metastasis ; Mitochondria ; Mitochondria - drug effects ; Mouth cancer ; Oral cancer ; p21Waf1/Cip1 ; Phosphorylation - drug effects ; Proteins ; Signal Transduction - drug effects ; STAT3 Transcription Factor - metabolism ; tannic acid ; Tannins ; Tannins - pharmacology</subject><ispartof>International journal of oncology, 2015-09, Vol.47 (3), p.1111-1120</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-bbbd6f4138a0b3046329e1f420ecd2780e4ae33d768e3ae919bfdd3116c5666b3</citedby><cites>FETCH-LOGICAL-c490t-bbbd6f4138a0b3046329e1f420ecd2780e4ae33d768e3ae919bfdd3116c5666b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26202061$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DARVIN, PRAMOD</creatorcontrib><creatorcontrib>BAEG, SEUNG JO</creatorcontrib><creatorcontrib>JOUNG, YOUN HEE</creatorcontrib><creatorcontrib>SP, NIPIN</creatorcontrib><creatorcontrib>KANG, DONG YOUNG</creatorcontrib><creatorcontrib>BYUN, HYO JOO</creatorcontrib><creatorcontrib>PARK, JE UK</creatorcontrib><creatorcontrib>YANG, YOUNG MOK</creatorcontrib><title>Tannic acid inhibits the Jak2/STAT3 pathway and induces G1/S arrest and mitochondrial apoptosis in YD-38 gingival cancer cells</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>Tannic acid (TA), is a potent anti-oxidant, showing anti-proliferative effects on numerous cancers. The ability of TA to induce proliferation inhibition on the rare tumor, gingival squamous cell carcinoma (GSCC), comprising <10% of all head and neck squamous cell carcinomas was studied in the YD-38 cell line. The main goal was to modulate the Jak2/STAT3 pathway using TA and to induce cell cycle arrest and apoptosis in GSCC. TA treatment induced G1 arrest and apoptosis in YD-38 cells. Molecular analysis revealed that TA inhibits Jak2/STAT3 pathway by preventing their expression as well as phosphorylation. This inhibition of STAT3 phosphorylation prevented the nuclear translocation and DNA binding capability of STAT3. Together with the inhibition of transcriptional regulatory function of STAT3, TA inhibited the expression of G1 phase modulators CDK-4, CDK-6, cyclin D1 and cyclin E. It is also evidenced that TA exerted an intense activation of p21Waf1/Cip1, p27Kip1 and p53 genes confirming its role in G1 phase inhibition. Additionally, upon treatment with TA, the expression of mitochondrial pore factors Bax, Bcl-2 and Bcl-XL were changed. We observed inhibition of Bcl-2 and an increase in mitochondrial localization of Bax leading to the loss of mitochondrial membrane potential, resulting in the release of cytochrome c to the cytosol. In addition, we perceived the activation of caspases upon TA treatment. Specific inhibition of caspase protected the cells from TA induced apoptosis. Taken together, this study reveals that TA significantly inhibits the Jak2/STAT3 signaling pathway and induces G1 arrest and mitochondrial apoptosis in YD-38 cells.</description><subject>Analysis</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Cancer</subject><subject>Carcinoma, Squamous Cell - drug therapy</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cytochrome</subject><subject>Drug therapy</subject><subject>G1 arrest</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genetic aspects</subject><subject>Gingival Neoplasms - drug therapy</subject><subject>Gingival Neoplasms - metabolism</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>intrinsic apoptosis</subject><subject>Jak2/STAT3</subject><subject>Janus Kinase 2 - metabolism</subject><subject>Kinases</subject><subject>Metastasis</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mouth cancer</subject><subject>Oral cancer</subject><subject>p21Waf1/Cip1</subject><subject>Phosphorylation - drug effects</subject><subject>Proteins</subject><subject>Signal Transduction - drug effects</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>tannic acid</subject><subject>Tannins</subject><subject>Tannins - pharmacology</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkc9vFCEUgCdGY2v16NWQmOiJXX4NMxw3tVZNEw9dD54IA8wO6wyMwGh66d8u69ZqE3kHyON7j0e-qnqJ0Yq2gqzdPqwIwvWKItE-qk5xIzAkjNDH5YywgJxRcVI9S2mPEKlrhJ9WJ4QTRBDHp9XtVnnvNFDaGeD84DqXE8iDBZ_UN7K-3m62FMwqDz_VDVD-wJhF2wQu8foaqBhtyr_zk8tBD8Gb6NQI1BzmHJJLhQdf30Hagp3zO_ej3GnltY1A23FMz6snvRqTfXG3n1Vf3l9szz_Aq8-XH883V1AzgTLsus7wnmHaKtRRxDglwuKeEWS1IU2LLFOWUtPw1lJlBRZdbwzFmOuac97Rs-r1se8cw_elzCz3YYm-PCmxoISSpuHiL7VTo5XO9yFHpSeXtNwwSlpRM1YXavUfqoSxk9PB296V_IOCN_8UDFaNeUhhXLILPj0E4RHUMaQUbS_n6CYVbyRG8mBbFtvyYFsebBf-1d2vlm6y5p7-o7cAb49AmosjZ0K6Z0onyBqIKMRl0V-c468V</recordid><startdate>20150901</startdate><enddate>20150901</enddate><creator>DARVIN, PRAMOD</creator><creator>BAEG, SEUNG JO</creator><creator>JOUNG, YOUN HEE</creator><creator>SP, NIPIN</creator><creator>KANG, DONG YOUNG</creator><creator>BYUN, HYO JOO</creator><creator>PARK, JE UK</creator><creator>YANG, YOUNG MOK</creator><general>D.A. 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The ability of TA to induce proliferation inhibition on the rare tumor, gingival squamous cell carcinoma (GSCC), comprising <10% of all head and neck squamous cell carcinomas was studied in the YD-38 cell line. The main goal was to modulate the Jak2/STAT3 pathway using TA and to induce cell cycle arrest and apoptosis in GSCC. TA treatment induced G1 arrest and apoptosis in YD-38 cells. Molecular analysis revealed that TA inhibits Jak2/STAT3 pathway by preventing their expression as well as phosphorylation. This inhibition of STAT3 phosphorylation prevented the nuclear translocation and DNA binding capability of STAT3. Together with the inhibition of transcriptional regulatory function of STAT3, TA inhibited the expression of G1 phase modulators CDK-4, CDK-6, cyclin D1 and cyclin E. It is also evidenced that TA exerted an intense activation of p21Waf1/Cip1, p27Kip1 and p53 genes confirming its role in G1 phase inhibition. Additionally, upon treatment with TA, the expression of mitochondrial pore factors Bax, Bcl-2 and Bcl-XL were changed. We observed inhibition of Bcl-2 and an increase in mitochondrial localization of Bax leading to the loss of mitochondrial membrane potential, resulting in the release of cytochrome c to the cytosol. In addition, we perceived the activation of caspases upon TA treatment. Specific inhibition of caspase protected the cells from TA induced apoptosis. Taken together, this study reveals that TA significantly inhibits the Jak2/STAT3 signaling pathway and induces G1 arrest and mitochondrial apoptosis in YD-38 cells.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>26202061</pmid><doi>10.3892/ijo.2015.3098</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of oncology, 2015-09, Vol.47 (3), p.1111-1120 |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Analysis Antineoplastic Agents - pharmacology Apoptosis Cancer Carcinoma, Squamous Cell - drug therapy Carcinoma, Squamous Cell - metabolism Cell cycle Cell Cycle - drug effects Cell growth Cell Line, Tumor Cytochrome Drug therapy G1 arrest Gene Expression Regulation, Neoplastic - drug effects Genetic aspects Gingival Neoplasms - drug therapy Gingival Neoplasms - metabolism Health aspects Humans Immunoglobulins intrinsic apoptosis Jak2/STAT3 Janus Kinase 2 - metabolism Kinases Metastasis Mitochondria Mitochondria - drug effects Mouth cancer Oral cancer p21Waf1/Cip1 Phosphorylation - drug effects Proteins Signal Transduction - drug effects STAT3 Transcription Factor - metabolism tannic acid Tannins Tannins - pharmacology |
| title | Tannic acid inhibits the Jak2/STAT3 pathway and induces G1/S arrest and mitochondrial apoptosis in YD-38 gingival cancer cells |
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