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β-Lapachone and its iodine derivatives cause cell cycle arrest at G 2 /M phase and reactive oxygen species-mediated apoptosis in human oral squamous cell carcinoma cells
β-Lapachone is a natural naphthoquinone originally obtained from the bark of the purple Ipe (Tabebuia avellanedae Lor, Bignoniaceae) and its therapeutic potential in human cancer cells has been evaluated in several studies. In this study, we examined the effects of β-lapachone and its 3-iodine deriv...
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| Published in: | Free radical biology & medicine 2018-10, Vol.126, p.87 |
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| creator | Dias, Rosane Borges de Araújo, Taís Bacelar Sacramento de Freitas, Raíza Dias Rodrigues, Ana Carolina Borges da Cruz Sousa, Letícia Palmeira Sales, Caroline Brandi Schlaepfer Valverde, Ludmila de Faro Soares, Milena Botelho Pereira Dos Reis, Mitermayer Galvão Coletta, Ricardo Della Ramos, Eduardo Antônio Gonçalves Camara, Celso Amorim Silva, Tania Maria Sarmento Filho, José Maria Barbosa Bezerra, Daniel Pereira Rocha, Clarissa Araújo Gurgel |
| description | β-Lapachone is a natural naphthoquinone originally obtained from the bark of the purple Ipe (Tabebuia avellanedae Lor, Bignoniaceae) and its therapeutic potential in human cancer cells has been evaluated in several studies. In this study, we examined the effects of β-lapachone and its 3-iodine derivatives (3-I-α-lapachone and 3-I-β-lapachone) on cell proliferation, cell death, and cancer-related gene expression in human oral squamous cell carcinoma cells. β-Lapachone and its 3-iodine derivatives showed potent cytotoxicity against different types of human cancer cell lines. Indeed, treatment with these compounds induced cell cycle arrest at G
/M phase, followed by internucleosomal DNA fragmentation, and caused significant increases in phosphatidylserine externalization, caspase-8 and -9 activation, mitochondrial membrane depolarization, reactive oxygen species (ROS) production, and apoptotic cell death morphology. The apoptosis induced by the compounds was prevented by pretreatment with a pan-caspase inhibitor (Z-VAD-FMK) and an antioxidant (N-acetyl-l-cysteine). In vivo, β-lapachone and its 3-iodine derivatives significantly reduced tumor burden and did not alter any of the biochemical, hematological, or histological parameters of the animals. Overall, β-lapachone and its 3-iodine derivatives showed promising cytotoxic activity due to their ability to induce cell cycle arrest at G
/M phase and promote caspase- and ROS-mediated apoptosis. In addition, β-lapachone and its 3-iodine derivatives were able to suppress tumor growth in vivo, indicating that these compounds may be new antitumor drug candidates. |
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/M phase, followed by internucleosomal DNA fragmentation, and caused significant increases in phosphatidylserine externalization, caspase-8 and -9 activation, mitochondrial membrane depolarization, reactive oxygen species (ROS) production, and apoptotic cell death morphology. The apoptosis induced by the compounds was prevented by pretreatment with a pan-caspase inhibitor (Z-VAD-FMK) and an antioxidant (N-acetyl-l-cysteine). In vivo, β-lapachone and its 3-iodine derivatives significantly reduced tumor burden and did not alter any of the biochemical, hematological, or histological parameters of the animals. Overall, β-lapachone and its 3-iodine derivatives showed promising cytotoxic activity due to their ability to induce cell cycle arrest at G
/M phase and promote caspase- and ROS-mediated apoptosis. In addition, β-lapachone and its 3-iodine derivatives were able to suppress tumor growth in vivo, indicating that these compounds may be new antitumor drug candidates.</description><identifier>EISSN: 1873-4596</identifier><identifier>PMID: 30071298</identifier><language>eng</language><publisher>United States</publisher><ispartof>Free radical biology & medicine, 2018-10, Vol.126, p.87</ispartof><rights>Copyright © 2018 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30071298$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dias, Rosane Borges</creatorcontrib><creatorcontrib>de Araújo, Taís Bacelar Sacramento</creatorcontrib><creatorcontrib>de Freitas, Raíza Dias</creatorcontrib><creatorcontrib>Rodrigues, Ana Carolina Borges da Cruz</creatorcontrib><creatorcontrib>Sousa, Letícia Palmeira</creatorcontrib><creatorcontrib>Sales, Caroline Brandi Schlaepfer</creatorcontrib><creatorcontrib>Valverde, Ludmila de Faro</creatorcontrib><creatorcontrib>Soares, Milena Botelho Pereira</creatorcontrib><creatorcontrib>Dos Reis, Mitermayer Galvão</creatorcontrib><creatorcontrib>Coletta, Ricardo Della</creatorcontrib><creatorcontrib>Ramos, Eduardo Antônio Gonçalves</creatorcontrib><creatorcontrib>Camara, Celso Amorim</creatorcontrib><creatorcontrib>Silva, Tania Maria Sarmento</creatorcontrib><creatorcontrib>Filho, José Maria Barbosa</creatorcontrib><creatorcontrib>Bezerra, Daniel Pereira</creatorcontrib><creatorcontrib>Rocha, Clarissa Araújo Gurgel</creatorcontrib><title>β-Lapachone and its iodine derivatives cause cell cycle arrest at G 2 /M phase and reactive oxygen species-mediated apoptosis in human oral squamous cell carcinoma cells</title><title>Free radical biology & medicine</title><addtitle>Free Radic Biol Med</addtitle><description>β-Lapachone is a natural naphthoquinone originally obtained from the bark of the purple Ipe (Tabebuia avellanedae Lor, Bignoniaceae) and its therapeutic potential in human cancer cells has been evaluated in several studies. In this study, we examined the effects of β-lapachone and its 3-iodine derivatives (3-I-α-lapachone and 3-I-β-lapachone) on cell proliferation, cell death, and cancer-related gene expression in human oral squamous cell carcinoma cells. β-Lapachone and its 3-iodine derivatives showed potent cytotoxicity against different types of human cancer cell lines. Indeed, treatment with these compounds induced cell cycle arrest at G
/M phase, followed by internucleosomal DNA fragmentation, and caused significant increases in phosphatidylserine externalization, caspase-8 and -9 activation, mitochondrial membrane depolarization, reactive oxygen species (ROS) production, and apoptotic cell death morphology. The apoptosis induced by the compounds was prevented by pretreatment with a pan-caspase inhibitor (Z-VAD-FMK) and an antioxidant (N-acetyl-l-cysteine). In vivo, β-lapachone and its 3-iodine derivatives significantly reduced tumor burden and did not alter any of the biochemical, hematological, or histological parameters of the animals. Overall, β-lapachone and its 3-iodine derivatives showed promising cytotoxic activity due to their ability to induce cell cycle arrest at G
/M phase and promote caspase- and ROS-mediated apoptosis. 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/M phase, followed by internucleosomal DNA fragmentation, and caused significant increases in phosphatidylserine externalization, caspase-8 and -9 activation, mitochondrial membrane depolarization, reactive oxygen species (ROS) production, and apoptotic cell death morphology. The apoptosis induced by the compounds was prevented by pretreatment with a pan-caspase inhibitor (Z-VAD-FMK) and an antioxidant (N-acetyl-l-cysteine). In vivo, β-lapachone and its 3-iodine derivatives significantly reduced tumor burden and did not alter any of the biochemical, hematological, or histological parameters of the animals. Overall, β-lapachone and its 3-iodine derivatives showed promising cytotoxic activity due to their ability to induce cell cycle arrest at G
/M phase and promote caspase- and ROS-mediated apoptosis. In addition, β-lapachone and its 3-iodine derivatives were able to suppress tumor growth in vivo, indicating that these compounds may be new antitumor drug candidates.</abstract><cop>United States</cop><pmid>30071298</pmid></addata></record> |
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| title | β-Lapachone and its iodine derivatives cause cell cycle arrest at G 2 /M phase and reactive oxygen species-mediated apoptosis in human oral squamous cell carcinoma cells |
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