Molecular pathways related to the control of proliferation and cell death in 786-O cells treated with plumbagin
Plumbagin (PLB) is a phytochemical being used for centuries in traditional medicines. Recently, its capacity to inhibit the development of human tumors has been observed, through the induction of apoptosis, cell cycle arrest, and inhibition of angiogenesis and metastasis. Here we evaluated the mecha...
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| Veröffentlicht in: | Molecular biology reports 2019-12, Vol.46 (6), p.6071-6078 |
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| creator | Mancilla, Igor Alves Coatti, Giuliana Castello Biazi, Bruna Isabela Zanetti, Thalita Alves Baranoski, Adrivanio Marques, Lilian Areal Corveloni, Amanda Cristina Lepri, Sandra Regina Mantovani, Mario Sergio |
| description | Plumbagin (PLB) is a phytochemical being used for centuries in traditional medicines. Recently, its capacity to inhibit the development of human tumors has been observed, through the induction of apoptosis, cell cycle arrest, and inhibition of angiogenesis and metastasis. Here we evaluated the mechanism of action of PLB in the kidney adenocarcinoma 786-O cell line, which are metabolizing cells important for toxicology studies. After the treatment with PLB, we observed increased apoptosis and cell cycle arrest in S and G2/M phases, starting at 5 µM. In addition, PLB was cytotoxic, genotoxic and induced loss of cell membrane integrity. Regarding gene expression, treatment with 7.5 µM PLB reduced the amount of
MTOR
,
BCL2
and
ATM
transcripts, and increased
CDKN1A
(p21) transcripts. Phosphorylation levels of yH2AX was increased and MDM2 protein level was reduced following the treatment with PLB, demonstrating its genotoxic effect. Our results suggest that PLB acts in molecular pathways related to the control of proliferation and cell death in 786-O cells. |
| doi_str_mv | 10.1007/s11033-019-05042-9 |
| format | Article |
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MTOR
,
BCL2
and
ATM
transcripts, and increased
CDKN1A
(p21) transcripts. Phosphorylation levels of yH2AX was increased and MDM2 protein level was reduced following the treatment with PLB, demonstrating its genotoxic effect. Our results suggest that PLB acts in molecular pathways related to the control of proliferation and cell death in 786-O cells.</description><identifier>ISSN: 0301-4851</identifier><identifier>EISSN: 1573-4978</identifier><identifier>DOI: 10.1007/s11033-019-05042-9</identifier><identifier>PMID: 31456160</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Adenocarcinoma ; Adenocarcinoma - metabolism ; Angiogenesis ; Animal Anatomy ; Animal Biochemistry ; Antineoplastic Agents - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Autophagy - drug effects ; Biomedical and Life Sciences ; Cell cycle ; cell cycle checkpoints ; Cell Cycle Checkpoints - drug effects ; Cell death ; Cell Death - drug effects ; Cell Line, Tumor - drug effects ; cell lines ; Cell membranes ; Cell proliferation ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cytotoxicity ; Gene expression ; Genotoxicity ; GTP-binding protein ; Histology ; Humans ; Kidney Neoplasms - metabolism ; kidneys ; Life Sciences ; MDM2 protein ; mechanism of action ; Metastases ; metastasis ; Morphology ; mutagens ; Naphthoquinones - metabolism ; Naphthoquinones - pharmacology ; Original Article ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphorylation ; phytochemicals ; Phytochemicals - metabolism ; Phytochemicals - pharmacology ; Plumbagin ; protein content ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction - drug effects ; TOR protein ; TOR Serine-Threonine Kinases - metabolism ; Tumors</subject><ispartof>Molecular biology reports, 2019-12, Vol.46 (6), p.6071-6078</ispartof><rights>Springer Nature B.V. 2019</rights><rights>Molecular Biology Reports is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-9c0a517bd7fd8e9e84a45b2cdeba4ba38b05b5851126a03193a122120bc2cd8f3</citedby><cites>FETCH-LOGICAL-c408t-9c0a517bd7fd8e9e84a45b2cdeba4ba38b05b5851126a03193a122120bc2cd8f3</cites><orcidid>0000-0001-5268-6508</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11033-019-05042-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11033-019-05042-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31456160$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mancilla, Igor Alves</creatorcontrib><creatorcontrib>Coatti, Giuliana Castello</creatorcontrib><creatorcontrib>Biazi, Bruna Isabela</creatorcontrib><creatorcontrib>Zanetti, Thalita Alves</creatorcontrib><creatorcontrib>Baranoski, Adrivanio</creatorcontrib><creatorcontrib>Marques, Lilian Areal</creatorcontrib><creatorcontrib>Corveloni, Amanda Cristina</creatorcontrib><creatorcontrib>Lepri, Sandra Regina</creatorcontrib><creatorcontrib>Mantovani, Mario Sergio</creatorcontrib><title>Molecular pathways related to the control of proliferation and cell death in 786-O cells treated with plumbagin</title><title>Molecular biology reports</title><addtitle>Mol Biol Rep</addtitle><addtitle>Mol Biol Rep</addtitle><description>Plumbagin (PLB) is a phytochemical being used for centuries in traditional medicines. Recently, its capacity to inhibit the development of human tumors has been observed, through the induction of apoptosis, cell cycle arrest, and inhibition of angiogenesis and metastasis. Here we evaluated the mechanism of action of PLB in the kidney adenocarcinoma 786-O cell line, which are metabolizing cells important for toxicology studies. After the treatment with PLB, we observed increased apoptosis and cell cycle arrest in S and G2/M phases, starting at 5 µM. In addition, PLB was cytotoxic, genotoxic and induced loss of cell membrane integrity. Regarding gene expression, treatment with 7.5 µM PLB reduced the amount of
MTOR
,
BCL2
and
ATM
transcripts, and increased
CDKN1A
(p21) transcripts. Phosphorylation levels of yH2AX was increased and MDM2 protein level was reduced following the treatment with PLB, demonstrating its genotoxic effect. Our results suggest that PLB acts in molecular pathways related to the control of proliferation and cell death in 786-O cells.</description><subject>Adenocarcinoma</subject><subject>Adenocarcinoma - metabolism</subject><subject>Angiogenesis</subject><subject>Animal Anatomy</subject><subject>Animal Biochemistry</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Autophagy - drug effects</subject><subject>Biomedical and Life Sciences</subject><subject>Cell cycle</subject><subject>cell cycle checkpoints</subject><subject>Cell Cycle Checkpoints - drug effects</subject><subject>Cell death</subject><subject>Cell Death - drug effects</subject><subject>Cell Line, Tumor - drug effects</subject><subject>cell lines</subject><subject>Cell membranes</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cytotoxicity</subject><subject>Gene expression</subject><subject>Genotoxicity</subject><subject>GTP-binding protein</subject><subject>Histology</subject><subject>Humans</subject><subject>Kidney Neoplasms - metabolism</subject><subject>kidneys</subject><subject>Life Sciences</subject><subject>MDM2 protein</subject><subject>mechanism of action</subject><subject>Metastases</subject><subject>metastasis</subject><subject>Morphology</subject><subject>mutagens</subject><subject>Naphthoquinones - metabolism</subject><subject>Naphthoquinones - pharmacology</subject><subject>Original Article</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphorylation</subject><subject>phytochemicals</subject><subject>Phytochemicals - metabolism</subject><subject>Phytochemicals - pharmacology</subject><subject>Plumbagin</subject><subject>protein content</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>TOR protein</subject><subject>TOR Serine-Threonine Kinases - metabolism</subject><subject>Tumors</subject><issn>0301-4851</issn><issn>1573-4978</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kUtP3DAUha2qVRmgf6CLylI3bAz3-pHYS4R4VAKxKWvLThwIysRT2xHi39fMQCuxYHUl3-8cH_sQ8h3hGAHak4wIQjBAw0CB5Mx8IitUrWDStPozWYEAZFIr3CP7OT8CgMRWfSV7AqVqsIEViTdxCt0yuUQ3rjw8uedMU5hcCT0tkZaHQLs4lxQnGge6qXMcQnJljDN1c0-7ME20D1VKx5m2umG327NMSwpbl6ex7jbTsvbufpwPyZfBTTl8e50H5O7i_PfZFbu-vfx1dnrNOgm6MNOBU9j6vh16HUzQ0knledcH76R3QntQXtWXIW8cCDTCIefIwXcV0oM4IEc73xr5zxJysesxvwRzc4hLtlwpNBIbrSr68x36GJc013SWcw1G6EbxSvEd1aWYcwqD3aRx7dKzRbAvddhdHbbWYbd1WFNFP16tF78O_T_J2_9XQOyAXFfzfUj_7_7A9i__xpUk</recordid><startdate>20191201</startdate><enddate>20191201</enddate><creator>Mancilla, Igor Alves</creator><creator>Coatti, Giuliana Castello</creator><creator>Biazi, Bruna Isabela</creator><creator>Zanetti, Thalita Alves</creator><creator>Baranoski, Adrivanio</creator><creator>Marques, Lilian Areal</creator><creator>Corveloni, Amanda Cristina</creator><creator>Lepri, Sandra Regina</creator><creator>Mantovani, Mario Sergio</creator><general>Springer Netherlands</general><general>Springer Nature B.V</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>3V.</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7S9</scope><scope>L.6</scope><orcidid>https://orcid.org/0000-0001-5268-6508</orcidid></search><sort><creationdate>20191201</creationdate><title>Molecular pathways related to the control of proliferation and cell death in 786-O cells treated with plumbagin</title><author>Mancilla, Igor Alves ; Coatti, Giuliana Castello ; Biazi, Bruna Isabela ; Zanetti, Thalita Alves ; Baranoski, Adrivanio ; Marques, Lilian Areal ; Corveloni, Amanda Cristina ; Lepri, Sandra Regina ; Mantovani, Mario Sergio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-9c0a517bd7fd8e9e84a45b2cdeba4ba38b05b5851126a03193a122120bc2cd8f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adenocarcinoma</topic><topic>Adenocarcinoma - metabolism</topic><topic>Angiogenesis</topic><topic>Animal Anatomy</topic><topic>Animal Biochemistry</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Autophagy - drug effects</topic><topic>Biomedical and Life Sciences</topic><topic>Cell cycle</topic><topic>cell cycle checkpoints</topic><topic>Cell Cycle Checkpoints - drug effects</topic><topic>Cell death</topic><topic>Cell Death - drug effects</topic><topic>Cell Line, Tumor - drug effects</topic><topic>cell lines</topic><topic>Cell membranes</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cytotoxicity</topic><topic>Gene expression</topic><topic>Genotoxicity</topic><topic>GTP-binding protein</topic><topic>Histology</topic><topic>Humans</topic><topic>Kidney Neoplasms - metabolism</topic><topic>kidneys</topic><topic>Life Sciences</topic><topic>MDM2 protein</topic><topic>mechanism of action</topic><topic>Metastases</topic><topic>metastasis</topic><topic>Morphology</topic><topic>mutagens</topic><topic>Naphthoquinones - metabolism</topic><topic>Naphthoquinones - pharmacology</topic><topic>Original Article</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphorylation</topic><topic>phytochemicals</topic><topic>Phytochemicals - metabolism</topic><topic>Phytochemicals - pharmacology</topic><topic>Plumbagin</topic><topic>protein content</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>TOR protein</topic><topic>TOR Serine-Threonine Kinases - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mancilla, Igor Alves</creatorcontrib><creatorcontrib>Coatti, Giuliana Castello</creatorcontrib><creatorcontrib>Biazi, Bruna Isabela</creatorcontrib><creatorcontrib>Zanetti, Thalita Alves</creatorcontrib><creatorcontrib>Baranoski, Adrivanio</creatorcontrib><creatorcontrib>Marques, Lilian Areal</creatorcontrib><creatorcontrib>Corveloni, Amanda Cristina</creatorcontrib><creatorcontrib>Lepri, Sandra Regina</creatorcontrib><creatorcontrib>Mantovani, Mario Sergio</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Molecular biology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mancilla, Igor Alves</au><au>Coatti, Giuliana Castello</au><au>Biazi, Bruna Isabela</au><au>Zanetti, Thalita Alves</au><au>Baranoski, Adrivanio</au><au>Marques, Lilian Areal</au><au>Corveloni, Amanda Cristina</au><au>Lepri, Sandra Regina</au><au>Mantovani, Mario Sergio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular pathways related to the control of proliferation and cell death in 786-O cells treated with plumbagin</atitle><jtitle>Molecular biology reports</jtitle><stitle>Mol Biol Rep</stitle><addtitle>Mol Biol Rep</addtitle><date>2019-12-01</date><risdate>2019</risdate><volume>46</volume><issue>6</issue><spage>6071</spage><epage>6078</epage><pages>6071-6078</pages><issn>0301-4851</issn><eissn>1573-4978</eissn><abstract>Plumbagin (PLB) is a phytochemical being used for centuries in traditional medicines. Recently, its capacity to inhibit the development of human tumors has been observed, through the induction of apoptosis, cell cycle arrest, and inhibition of angiogenesis and metastasis. Here we evaluated the mechanism of action of PLB in the kidney adenocarcinoma 786-O cell line, which are metabolizing cells important for toxicology studies. After the treatment with PLB, we observed increased apoptosis and cell cycle arrest in S and G2/M phases, starting at 5 µM. In addition, PLB was cytotoxic, genotoxic and induced loss of cell membrane integrity. Regarding gene expression, treatment with 7.5 µM PLB reduced the amount of
MTOR
,
BCL2
and
ATM
transcripts, and increased
CDKN1A
(p21) transcripts. Phosphorylation levels of yH2AX was increased and MDM2 protein level was reduced following the treatment with PLB, demonstrating its genotoxic effect. Our results suggest that PLB acts in molecular pathways related to the control of proliferation and cell death in 786-O cells.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>31456160</pmid><doi>10.1007/s11033-019-05042-9</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-5268-6508</orcidid></addata></record> |
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| ispartof | Molecular biology reports, 2019-12, Vol.46 (6), p.6071-6078 |
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| subjects | Adenocarcinoma Adenocarcinoma - metabolism Angiogenesis Animal Anatomy Animal Biochemistry Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Autophagy - drug effects Biomedical and Life Sciences Cell cycle cell cycle checkpoints Cell Cycle Checkpoints - drug effects Cell death Cell Death - drug effects Cell Line, Tumor - drug effects cell lines Cell membranes Cell proliferation Cell Proliferation - drug effects Cell Survival - drug effects Cytotoxicity Gene expression Genotoxicity GTP-binding protein Histology Humans Kidney Neoplasms - metabolism kidneys Life Sciences MDM2 protein mechanism of action Metastases metastasis Morphology mutagens Naphthoquinones - metabolism Naphthoquinones - pharmacology Original Article p38 Mitogen-Activated Protein Kinases - metabolism Phosphatidylinositol 3-Kinases - metabolism Phosphorylation phytochemicals Phytochemicals - metabolism Phytochemicals - pharmacology Plumbagin protein content Proto-Oncogene Proteins c-akt - metabolism Signal Transduction - drug effects TOR protein TOR Serine-Threonine Kinases - metabolism Tumors |
| title | Molecular pathways related to the control of proliferation and cell death in 786-O cells treated with plumbagin |
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