Dioscin facilitates ROS-induced apoptosis via the p38-MAPK/HSP27-mediated pathways in lung squamous cell carcinoma
Lung squamous cell carcinoma (SCC) is one of the deadliest cancers both in China and worldwide. To date, the efficacy of lung SCC treatments is limited. Recent studies have elucidated the powerful anti-tumour role of dioscin in different human cancers. Here, our study aims to investigate the effect...
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| Veröffentlicht in: | International journal of biological sciences 2020-01, Vol.16 (15), p.2883-2894 |
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| creator | Yao, Yinan Cui, Luyun Ye, Jiani Yang, Guangdie Lu, Guohua Fang, Xiaomei Zeng, Zhu Zhou, Jianying |
| description | Lung squamous cell carcinoma (SCC) is one of the deadliest cancers both in China and worldwide. To date, the efficacy of lung SCC treatments is limited. Recent studies have elucidated the powerful anti-tumour role of dioscin in different human cancers. Here, our study aims to investigate the effect of dioscin on lung SCC and its underlying mechanism. First, we found that dioscin not only inhibited cell proliferation and cell migration and induced cell apoptosis in lung SCC cells but also suppressed tumour growth in tumour-bearing mice. Furthermore, we noted that the accumulation of intracellular reactive oxygen species (ROS) was triggered by dioscin in lung SCC cells, leading to the phosphorylation of HSP27 through p38-MAPK and consequent cell apoptosis. The activation of p38-MAPK/HSP27 induced by the p38-MAPK activator Anisomycin enhanced the apoptosis of lung SCC cells, while the ROS inhibitor N-acetyl-L-cysteine (NAC) and the p38-MAPK inhibitor SB203580 both attenuated dioscin-mediated cell apoptosis. Moreover, NAC suppressed the activation of p38-MAPK/HSP27 that induced by dioscin. In conclusion, these results confirm that dioscin facilitates ROS-induced apoptosis via the p38-MAPK/HSP27-mediated pathway in lung SCC. |
| doi_str_mv | 10.7150/ijbs.45710 |
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To date, the efficacy of lung SCC treatments is limited. Recent studies have elucidated the powerful anti-tumour role of dioscin in different human cancers. Here, our study aims to investigate the effect of dioscin on lung SCC and its underlying mechanism. First, we found that dioscin not only inhibited cell proliferation and cell migration and induced cell apoptosis in lung SCC cells but also suppressed tumour growth in tumour-bearing mice. Furthermore, we noted that the accumulation of intracellular reactive oxygen species (ROS) was triggered by dioscin in lung SCC cells, leading to the phosphorylation of HSP27 through p38-MAPK and consequent cell apoptosis. The activation of p38-MAPK/HSP27 induced by the p38-MAPK activator Anisomycin enhanced the apoptosis of lung SCC cells, while the ROS inhibitor N-acetyl-L-cysteine (NAC) and the p38-MAPK inhibitor SB203580 both attenuated dioscin-mediated cell apoptosis. Moreover, NAC suppressed the activation of p38-MAPK/HSP27 that induced by dioscin. In conclusion, these results confirm that dioscin facilitates ROS-induced apoptosis via the p38-MAPK/HSP27-mediated pathway in lung SCC.</description><identifier>ISSN: 1449-2288</identifier><identifier>EISSN: 1449-2288</identifier><identifier>DOI: 10.7150/ijbs.45710</identifier><identifier>PMID: 33061803</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>Acetylcysteine ; Animals ; Anisomycin ; Antibodies ; Apoptosis ; Biotechnology ; Cancer ; Cancer therapies ; Carcinoma, Squamous Cell - drug therapy ; Cell activation ; Cell cycle ; Cell migration ; Cell proliferation ; Diosgenin - analogs & derivatives ; DNA damage ; HSP27 Heat-Shock Proteins - metabolism ; HSP27 Heat-Shock Proteins - pharmacology ; Hsp27 protein ; Inhibitors ; Lung - metabolism ; Lung cancer ; Lung carcinoma ; Lungs ; MAP kinase ; Mice ; N-Acetyl-L-cysteine ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phosphorylation ; Proteins ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Research Paper ; Squamous cell carcinoma ; Tumors</subject><ispartof>International journal of biological sciences, 2020-01, Vol.16 (15), p.2883-2894</ispartof><rights>The author(s).</rights><rights>2020. 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To date, the efficacy of lung SCC treatments is limited. Recent studies have elucidated the powerful anti-tumour role of dioscin in different human cancers. Here, our study aims to investigate the effect of dioscin on lung SCC and its underlying mechanism. First, we found that dioscin not only inhibited cell proliferation and cell migration and induced cell apoptosis in lung SCC cells but also suppressed tumour growth in tumour-bearing mice. Furthermore, we noted that the accumulation of intracellular reactive oxygen species (ROS) was triggered by dioscin in lung SCC cells, leading to the phosphorylation of HSP27 through p38-MAPK and consequent cell apoptosis. The activation of p38-MAPK/HSP27 induced by the p38-MAPK activator Anisomycin enhanced the apoptosis of lung SCC cells, while the ROS inhibitor N-acetyl-L-cysteine (NAC) and the p38-MAPK inhibitor SB203580 both attenuated dioscin-mediated cell apoptosis. 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In conclusion, these results confirm that dioscin facilitates ROS-induced apoptosis via the p38-MAPK/HSP27-mediated pathway in lung SCC.</description><subject>Acetylcysteine</subject><subject>Animals</subject><subject>Anisomycin</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Biotechnology</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Carcinoma, Squamous Cell - drug therapy</subject><subject>Cell activation</subject><subject>Cell cycle</subject><subject>Cell migration</subject><subject>Cell proliferation</subject><subject>Diosgenin - analogs & derivatives</subject><subject>DNA damage</subject><subject>HSP27 Heat-Shock Proteins - metabolism</subject><subject>HSP27 Heat-Shock Proteins - pharmacology</subject><subject>Hsp27 protein</subject><subject>Inhibitors</subject><subject>Lung - metabolism</subject><subject>Lung cancer</subject><subject>Lung carcinoma</subject><subject>Lungs</subject><subject>MAP kinase</subject><subject>Mice</subject><subject>N-Acetyl-L-cysteine</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Research Paper</subject><subject>Squamous cell carcinoma</subject><subject>Tumors</subject><issn>1449-2288</issn><issn>1449-2288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNpdkVtLHTEUhYNYvLUv_oAS8EUKo7lOcl4Kom0ttSi1Poc9ScaTw8xkTGYU_7051YrtUwL5svZaeyG0T8mRopIch1WTj4RUlGygHSrEomJM68039220m_OKEF5LTbbQNuekpprwHZTOQsw2DLgFG7owweQz_nV5XYXBzdY7DGMcp5hDxvcB8LT0eOS6-nly9eP4_PqKqar3LpRfDo8wLR_gMeOi1s3DLc53M_Rxztj6rsMWUpkTe3iP3rXQZf_h5dxDN1-__D49ry4uv30_PbmorCD1VNmF47XWjraOt6qVFLTQjdXaC6uF4oQIa8HWsoFaAwfPG99ypTzjzDGn-R76_Kw7zk0xaf0wJejMmEIP6dFECObflyEszW28N0qWZRJVBA5fBFK8m32eTB_yOgsMvsQyTEiq5ULVpKAH_6GrOKehxDNMLrQgjDJWqE_PlE0x5-TbVzOUmHWVZl2l-VNlgT--tf-K_u2OPwHjnpsn</recordid><startdate>20200101</startdate><enddate>20200101</enddate><creator>Yao, Yinan</creator><creator>Cui, Luyun</creator><creator>Ye, Jiani</creator><creator>Yang, Guangdie</creator><creator>Lu, Guohua</creator><creator>Fang, Xiaomei</creator><creator>Zeng, Zhu</creator><creator>Zhou, Jianying</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</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>7QL</scope><scope>7QO</scope><scope>7U9</scope><scope>8FD</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20200101</creationdate><title>Dioscin facilitates ROS-induced apoptosis via the p38-MAPK/HSP27-mediated pathways in lung squamous cell carcinoma</title><author>Yao, Yinan ; 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To date, the efficacy of lung SCC treatments is limited. Recent studies have elucidated the powerful anti-tumour role of dioscin in different human cancers. Here, our study aims to investigate the effect of dioscin on lung SCC and its underlying mechanism. First, we found that dioscin not only inhibited cell proliferation and cell migration and induced cell apoptosis in lung SCC cells but also suppressed tumour growth in tumour-bearing mice. Furthermore, we noted that the accumulation of intracellular reactive oxygen species (ROS) was triggered by dioscin in lung SCC cells, leading to the phosphorylation of HSP27 through p38-MAPK and consequent cell apoptosis. The activation of p38-MAPK/HSP27 induced by the p38-MAPK activator Anisomycin enhanced the apoptosis of lung SCC cells, while the ROS inhibitor N-acetyl-L-cysteine (NAC) and the p38-MAPK inhibitor SB203580 both attenuated dioscin-mediated cell apoptosis. Moreover, NAC suppressed the activation of p38-MAPK/HSP27 that induced by dioscin. In conclusion, these results confirm that dioscin facilitates ROS-induced apoptosis via the p38-MAPK/HSP27-mediated pathway in lung SCC.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>33061803</pmid><doi>10.7150/ijbs.45710</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acetylcysteine Animals Anisomycin Antibodies Apoptosis Biotechnology Cancer Cancer therapies Carcinoma, Squamous Cell - drug therapy Cell activation Cell cycle Cell migration Cell proliferation Diosgenin - analogs & derivatives DNA damage HSP27 Heat-Shock Proteins - metabolism HSP27 Heat-Shock Proteins - pharmacology Hsp27 protein Inhibitors Lung - metabolism Lung cancer Lung carcinoma Lungs MAP kinase Mice N-Acetyl-L-cysteine p38 Mitogen-Activated Protein Kinases - metabolism Phosphorylation Proteins Reactive oxygen species Reactive Oxygen Species - metabolism Research Paper Squamous cell carcinoma Tumors |
| title | Dioscin facilitates ROS-induced apoptosis via the p38-MAPK/HSP27-mediated pathways in lung squamous cell carcinoma |
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