Propranolol induced apoptosis and autophagy via the ROS/JNK signaling pathway in Human Ovarian Cancer
Propranolol has a significant anti-cancer effect towards various cancers. Our study aimed at investigating the underlying mechanism of Propranolol's therapeutic effect towards ovarian cancer. Specifically, Propranolol significantly reduced the viability of human ovarian cancer cell lines SKOV-3...
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| Veröffentlicht in: | Journal of Cancer 2020-01, Vol.11 (20), p.5900-5910 |
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| container_title | Journal of Cancer |
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| creator | Zhao, Shujun Fan, Suzhen Shi, Yanyu Ren, Hongyan Hong, Hanqing Gao, Xiang Zhang, Min Qin, Qiaohong Li, Hongyu |
| description | Propranolol has a significant anti-cancer effect towards various cancers. Our study aimed at investigating the underlying mechanism of Propranolol's therapeutic effect towards ovarian cancer. Specifically, Propranolol significantly reduced the viability of human ovarian cancer cell lines SKOV-3 and A2780 in a dose- and time-dependent manner. Flow cytometry analysis revealed that Propranolol induced the cell cycle arrest at G2/M phase therefore leading to apoptosis. Moreover, autophagy inhibitor 3-MA markedly enhanced the Propranolol-induced apoptosis. In addition, reactive oxygen species (ROS) increased dramatically after Propranolol treatment and Propranolol activated the phosphorylation of JNK. What is more, p38 inhibitor SB203580 and JNK inhibitor SP600125 attenuated the upregulated expression of LC3-II and cleaved-caspase-3 by the effect of Propranolol. ROS exclusive inhibitor antioxidant N-acetyl cysteine (NAC) weakens the phosphorylation of JNK proteins induced by Propranolol. In summary, these results suggested that Propranolol induced cell apoptosis and protective autophagy through the ROS/JNK signaling pathway in human ovarian cancer cells. |
| doi_str_mv | 10.7150/jca.46556 |
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Our study aimed at investigating the underlying mechanism of Propranolol's therapeutic effect towards ovarian cancer. Specifically, Propranolol significantly reduced the viability of human ovarian cancer cell lines SKOV-3 and A2780 in a dose- and time-dependent manner. Flow cytometry analysis revealed that Propranolol induced the cell cycle arrest at G2/M phase therefore leading to apoptosis. Moreover, autophagy inhibitor 3-MA markedly enhanced the Propranolol-induced apoptosis. In addition, reactive oxygen species (ROS) increased dramatically after Propranolol treatment and Propranolol activated the phosphorylation of JNK. What is more, p38 inhibitor SB203580 and JNK inhibitor SP600125 attenuated the upregulated expression of LC3-II and cleaved-caspase-3 by the effect of Propranolol. ROS exclusive inhibitor antioxidant N-acetyl cysteine (NAC) weakens the phosphorylation of JNK proteins induced by Propranolol. In summary, these results suggested that Propranolol induced cell apoptosis and protective autophagy through the ROS/JNK signaling pathway in human ovarian cancer cells.</description><identifier>ISSN: 1837-9664</identifier><identifier>EISSN: 1837-9664</identifier><identifier>DOI: 10.7150/jca.46556</identifier><identifier>PMID: 32922532</identifier><language>eng</language><publisher>Wyoming: Ivyspring International Publisher Pty Ltd</publisher><subject>Antibodies ; Apoptosis ; Autophagy ; Biotechnology ; Cancer therapies ; Cell cycle ; Kinases ; Ovarian cancer ; Proteins ; Reactive oxygen species ; Research Paper ; Statistical analysis ; Womens health</subject><ispartof>Journal of Cancer, 2020-01, Vol.11 (20), p.5900-5910</ispartof><rights>2020. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The author(s) 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c380t-af62c77407e81ba561174fab03551b1de12e28cc033d26c290ec1f8f564dd06f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7477428/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7477428/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids></links><search><creatorcontrib>Zhao, Shujun</creatorcontrib><creatorcontrib>Fan, Suzhen</creatorcontrib><creatorcontrib>Shi, Yanyu</creatorcontrib><creatorcontrib>Ren, Hongyan</creatorcontrib><creatorcontrib>Hong, Hanqing</creatorcontrib><creatorcontrib>Gao, Xiang</creatorcontrib><creatorcontrib>Zhang, Min</creatorcontrib><creatorcontrib>Qin, Qiaohong</creatorcontrib><creatorcontrib>Li, Hongyu</creatorcontrib><title>Propranolol induced apoptosis and autophagy via the ROS/JNK signaling pathway in Human Ovarian Cancer</title><title>Journal of Cancer</title><description>Propranolol has a significant anti-cancer effect towards various cancers. 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In summary, these results suggested that Propranolol induced cell apoptosis and protective autophagy through the ROS/JNK signaling pathway in human ovarian cancer cells.</description><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Biotechnology</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Kinases</subject><subject>Ovarian cancer</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Research Paper</subject><subject>Statistical analysis</subject><subject>Womens health</subject><issn>1837-9664</issn><issn>1837-9664</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNpdkU1PGzEQhq2qqCDg0H9gqZf2EOJv714qoQhICyKo0LM18XoTRxt7sXeD8u_rFlQBc5kZzaN3RvMi9JmSM00lmW4snAklpfqAjmjF9aRWSnx8VR-i05w3pASvmRb8EzrkrGZMcnaE3F2KfYIQu9hhH5rRugZDH_shZp8xhNKNQ-zXsNrjnQc8rB3-tbif_ry9xtmvAnQ-rHAPw_oJ9kUBz8ctBLzYQfIlzyBYl07QQQtddqcv-Rj9vrx4mM0nN4urH7Pzm4nlFRkm0CpmtRZEu4ouQSpKtWhhSbiUdEkbR5ljlbWE84Ypy2riLG2rVirRNES1_Bh9f9btx-XWNdaFIUFn-uS3kPYmgjdvJ8GvzSrujBZlLauKwNcXgRQfR5cHs_XZuq6D4OKYDROCyVpKzQv65R26iWMq_yiUrCvOdEVpob49UzbFnJNr_x9Difnrnyn-mX_-8T_J8ox_</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Zhao, Shujun</creator><creator>Fan, Suzhen</creator><creator>Shi, Yanyu</creator><creator>Ren, Hongyan</creator><creator>Hong, Hanqing</creator><creator>Gao, Xiang</creator><creator>Zhang, Min</creator><creator>Qin, Qiaohong</creator><creator>Li, Hongyu</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200101</creationdate><title>Propranolol induced apoptosis and autophagy via the ROS/JNK signaling pathway in Human Ovarian Cancer</title><author>Zhao, Shujun ; 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Our study aimed at investigating the underlying mechanism of Propranolol's therapeutic effect towards ovarian cancer. Specifically, Propranolol significantly reduced the viability of human ovarian cancer cell lines SKOV-3 and A2780 in a dose- and time-dependent manner. Flow cytometry analysis revealed that Propranolol induced the cell cycle arrest at G2/M phase therefore leading to apoptosis. Moreover, autophagy inhibitor 3-MA markedly enhanced the Propranolol-induced apoptosis. In addition, reactive oxygen species (ROS) increased dramatically after Propranolol treatment and Propranolol activated the phosphorylation of JNK. What is more, p38 inhibitor SB203580 and JNK inhibitor SP600125 attenuated the upregulated expression of LC3-II and cleaved-caspase-3 by the effect of Propranolol. ROS exclusive inhibitor antioxidant N-acetyl cysteine (NAC) weakens the phosphorylation of JNK proteins induced by Propranolol. 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| subjects | Antibodies Apoptosis Autophagy Biotechnology Cancer therapies Cell cycle Kinases Ovarian cancer Proteins Reactive oxygen species Research Paper Statistical analysis Womens health |
| title | Propranolol induced apoptosis and autophagy via the ROS/JNK signaling pathway in Human Ovarian Cancer |
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