Epieriocalyxin A Induces Cell Apoptosis Through JNK and ERK1/2 Signaling Pathways in Colon Cancer Cells
Colorectal cancer is one of the most commonly diagnosed cancers in the world. Currently, drug resistance of cancer cell to chemotherapy is a major cause for cancer recurrence and death of the patients; therefore, new therapeutic strategy is required to improve the care of colorectal cancer patients....
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| Veröffentlicht in: | Cell biochemistry and biophysics 2015-11, Vol.73 (2), p.559-564 |
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| creator | Wang, Zhou Xu, Zhijie Niu, Zhengchuan Liang, Benjia Niu, Jun |
| description | Colorectal cancer is one of the most commonly diagnosed cancers in the world. Currently, drug resistance of cancer cell to chemotherapy is a major cause for cancer recurrence and death of the patients; therefore, new therapeutic strategy is required to improve the care of colorectal cancer patients. The Chinese herb,
Isodon eriocalyx
, has been used a therapeutic for a long time in China. In this study, we showed that Epieriocalyxin A (EpiA), a diterpenoid isolated from
I
.
eriocalyx
, suppressed Caco-2 colon cancer cell growth. EpiA induced annexin V flipping in cell membrane and DNA fragment. We also showed that EpiA induced the generation of ROS in cells, as well as damage of the mitochondrial membrane. Western blot results showed that both JNK and ERK1/2 activation was decreased after EpiA treatment in a dose-dependent manner. EpiA increased the expression of caspase 3 and Bax, and decreased Bcl2 expression. Our results suggest that EpiA is a novel compound that induces colon cancer apoptosis. EpiA could be a potential drug for colon cancer therapy in the future. |
| doi_str_mv | 10.1007/s12013-015-0687-4 |
| format | Article |
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Isodon eriocalyx
, has been used a therapeutic for a long time in China. In this study, we showed that Epieriocalyxin A (EpiA), a diterpenoid isolated from
I
.
eriocalyx
, suppressed Caco-2 colon cancer cell growth. EpiA induced annexin V flipping in cell membrane and DNA fragment. We also showed that EpiA induced the generation of ROS in cells, as well as damage of the mitochondrial membrane. Western blot results showed that both JNK and ERK1/2 activation was decreased after EpiA treatment in a dose-dependent manner. EpiA increased the expression of caspase 3 and Bax, and decreased Bcl2 expression. Our results suggest that EpiA is a novel compound that induces colon cancer apoptosis. EpiA could be a potential drug for colon cancer therapy in the future.</description><identifier>ISSN: 1085-9195</identifier><identifier>EISSN: 1559-0283</identifier><identifier>DOI: 10.1007/s12013-015-0687-4</identifier><identifier>PMID: 27352353</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Apoptosis - drug effects ; bcl-2-Associated X Protein - metabolism ; Biochemistry ; Biological and Medical Physics ; Biomedical and Life Sciences ; Biophysics ; Biotechnology ; Blotting, Western ; Caco-2 Cells ; Caspase 3 - metabolism ; Cell Biology ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - pathology ; Colorectal carcinoma ; Diterpenes - chemistry ; Diterpenes - toxicity ; DNA Fragmentation - drug effects ; Down-Regulation - drug effects ; Drug resistance ; Humans ; Isodon - chemistry ; Isodon - metabolism ; JNK Mitogen-Activated Protein Kinases - metabolism ; Life Sciences ; Membrane Potential, Mitochondrial - drug effects ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - metabolism ; Original Paper ; Pharmacology/Toxicology ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Reactive Oxygen Species - metabolism ; Signal Transduction - drug effects</subject><ispartof>Cell biochemistry and biophysics, 2015-11, Vol.73 (2), p.559-564</ispartof><rights>Springer Science+Business Media New York 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-9282708afdf4874726b67c4868d7a175ebf73f5c00cd3af0a6c4f10a8a3181433</citedby><cites>FETCH-LOGICAL-c405t-9282708afdf4874726b67c4868d7a175ebf73f5c00cd3af0a6c4f10a8a3181433</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12013-015-0687-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12013-015-0687-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27352353$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Zhou</creatorcontrib><creatorcontrib>Xu, Zhijie</creatorcontrib><creatorcontrib>Niu, Zhengchuan</creatorcontrib><creatorcontrib>Liang, Benjia</creatorcontrib><creatorcontrib>Niu, Jun</creatorcontrib><title>Epieriocalyxin A Induces Cell Apoptosis Through JNK and ERK1/2 Signaling Pathways in Colon Cancer Cells</title><title>Cell biochemistry and biophysics</title><addtitle>Cell Biochem Biophys</addtitle><addtitle>Cell Biochem Biophys</addtitle><description>Colorectal cancer is one of the most commonly diagnosed cancers in the world. Currently, drug resistance of cancer cell to chemotherapy is a major cause for cancer recurrence and death of the patients; therefore, new therapeutic strategy is required to improve the care of colorectal cancer patients. The Chinese herb,
Isodon eriocalyx
, has been used a therapeutic for a long time in China. In this study, we showed that Epieriocalyxin A (EpiA), a diterpenoid isolated from
I
.
eriocalyx
, suppressed Caco-2 colon cancer cell growth. EpiA induced annexin V flipping in cell membrane and DNA fragment. We also showed that EpiA induced the generation of ROS in cells, as well as damage of the mitochondrial membrane. Western blot results showed that both JNK and ERK1/2 activation was decreased after EpiA treatment in a dose-dependent manner. EpiA increased the expression of caspase 3 and Bax, and decreased Bcl2 expression. Our results suggest that EpiA is a novel compound that induces colon cancer apoptosis. EpiA could be a potential drug for colon cancer therapy in the future.</description><subject>Apoptosis - drug effects</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Biochemistry</subject><subject>Biological and Medical Physics</subject><subject>Biomedical and Life Sciences</subject><subject>Biophysics</subject><subject>Biotechnology</subject><subject>Blotting, Western</subject><subject>Caco-2 Cells</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Biology</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colonic Neoplasms - pathology</subject><subject>Colorectal carcinoma</subject><subject>Diterpenes - chemistry</subject><subject>Diterpenes - toxicity</subject><subject>DNA Fragmentation - drug effects</subject><subject>Down-Regulation - drug effects</subject><subject>Drug resistance</subject><subject>Humans</subject><subject>Isodon - chemistry</subject><subject>Isodon - metabolism</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>Life Sciences</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Original Paper</subject><subject>Pharmacology/Toxicology</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Signal Transduction - drug effects</subject><issn>1085-9195</issn><issn>1559-0283</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</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><sourceid>GNUQQ</sourceid><recordid>eNp1kU1v1DAQhq2Kin7AD-gFWeLCJXTGH7FzXK0WWlpBBeVseR0nmyobB3ujdv893m5bVUhcbEt-5hl7XkLOED4jgDpPyAB5ASgLKLUqxAE5RimrApjmb_IZtCwqrOQROUnpDoAxEOItOWKKS8YlPybtYux87IKz_fahG-iMXg715Hyic9_3dDaGcRNSl-jtKoapXdFv36-oHWq6-HmF54z-6trB9t3Q0hu7Wd3bbaLZMg99yKsdnI-PovSOHDa2T_79035Kfn9Z3M4viusfXy_ns-vCCZCbomKaKdC2qRuhlVCsXJbKCV3qWllU0i8bxRvpAFzNbQO2dKJBsNpy1Cg4PyWf9t4xhj-TTxuz7pLLL7CDD1MyqPPgACtRZfTjP-hdmGL-TaYUqkrl7iJTuKdcDClF35gxdmsbtwbB7FIw-xRMTsHsUjC7mg9P5mm59vVLxfPYM8D2QMpXQ-vjq9b_tf4FHc6Peg</recordid><startdate>20151101</startdate><enddate>20151101</enddate><creator>Wang, Zhou</creator><creator>Xu, Zhijie</creator><creator>Niu, Zhengchuan</creator><creator>Liang, Benjia</creator><creator>Niu, Jun</creator><general>Springer US</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>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</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>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20151101</creationdate><title>Epieriocalyxin A Induces Cell Apoptosis Through JNK and ERK1/2 Signaling Pathways in Colon Cancer Cells</title><author>Wang, Zhou ; Xu, Zhijie ; Niu, Zhengchuan ; Liang, Benjia ; Niu, Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-9282708afdf4874726b67c4868d7a175ebf73f5c00cd3af0a6c4f10a8a3181433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Apoptosis - drug effects</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Biochemistry</topic><topic>Biological and Medical Physics</topic><topic>Biomedical and Life Sciences</topic><topic>Biophysics</topic><topic>Biotechnology</topic><topic>Blotting, Western</topic><topic>Caco-2 Cells</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Biology</topic><topic>Colonic Neoplasms - metabolism</topic><topic>Colonic Neoplasms - pathology</topic><topic>Colorectal carcinoma</topic><topic>Diterpenes - chemistry</topic><topic>Diterpenes - toxicity</topic><topic>DNA Fragmentation - drug effects</topic><topic>Down-Regulation - drug effects</topic><topic>Drug resistance</topic><topic>Humans</topic><topic>Isodon - chemistry</topic><topic>Isodon - metabolism</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>Life Sciences</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Original Paper</topic><topic>Pharmacology/Toxicology</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Signal Transduction - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Zhou</creatorcontrib><creatorcontrib>Xu, Zhijie</creatorcontrib><creatorcontrib>Niu, Zhengchuan</creatorcontrib><creatorcontrib>Liang, Benjia</creatorcontrib><creatorcontrib>Niu, Jun</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS 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>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>Environmental Sciences and Pollution Management</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>AIDS and Cancer Research Abstracts</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>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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell biochemistry and biophysics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Zhou</au><au>Xu, Zhijie</au><au>Niu, Zhengchuan</au><au>Liang, Benjia</au><au>Niu, Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epieriocalyxin A Induces Cell Apoptosis Through JNK and ERK1/2 Signaling Pathways in Colon Cancer Cells</atitle><jtitle>Cell biochemistry and biophysics</jtitle><stitle>Cell Biochem Biophys</stitle><addtitle>Cell Biochem Biophys</addtitle><date>2015-11-01</date><risdate>2015</risdate><volume>73</volume><issue>2</issue><spage>559</spage><epage>564</epage><pages>559-564</pages><issn>1085-9195</issn><eissn>1559-0283</eissn><abstract>Colorectal cancer is one of the most commonly diagnosed cancers in the world. Currently, drug resistance of cancer cell to chemotherapy is a major cause for cancer recurrence and death of the patients; therefore, new therapeutic strategy is required to improve the care of colorectal cancer patients. The Chinese herb,
Isodon eriocalyx
, has been used a therapeutic for a long time in China. In this study, we showed that Epieriocalyxin A (EpiA), a diterpenoid isolated from
I
.
eriocalyx
, suppressed Caco-2 colon cancer cell growth. EpiA induced annexin V flipping in cell membrane and DNA fragment. We also showed that EpiA induced the generation of ROS in cells, as well as damage of the mitochondrial membrane. Western blot results showed that both JNK and ERK1/2 activation was decreased after EpiA treatment in a dose-dependent manner. EpiA increased the expression of caspase 3 and Bax, and decreased Bcl2 expression. Our results suggest that EpiA is a novel compound that induces colon cancer apoptosis. EpiA could be a potential drug for colon cancer therapy in the future.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>27352353</pmid><doi>10.1007/s12013-015-0687-4</doi><tpages>6</tpages></addata></record> |
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| subjects | Apoptosis - drug effects bcl-2-Associated X Protein - metabolism Biochemistry Biological and Medical Physics Biomedical and Life Sciences Biophysics Biotechnology Blotting, Western Caco-2 Cells Caspase 3 - metabolism Cell Biology Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Colorectal carcinoma Diterpenes - chemistry Diterpenes - toxicity DNA Fragmentation - drug effects Down-Regulation - drug effects Drug resistance Humans Isodon - chemistry Isodon - metabolism JNK Mitogen-Activated Protein Kinases - metabolism Life Sciences Membrane Potential, Mitochondrial - drug effects Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - metabolism Original Paper Pharmacology/Toxicology Proto-Oncogene Proteins c-bcl-2 - metabolism Reactive Oxygen Species - metabolism Signal Transduction - drug effects |
| title | Epieriocalyxin A Induces Cell Apoptosis Through JNK and ERK1/2 Signaling Pathways in Colon Cancer Cells |
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