Roles of p38 and JNK protein kinase pathways activated by compound cantharidin capsules containing serum on proliferation inhibition and apoptosis of human gastric cancer cell line
The aim of the present study was to investigate the inhibitory effect of compound cantharides capsules (CCCs) on the viability and apoptosis of human gastric cancer cell lines, BGC-823 and SGC-7901, and to detect its regulation of gene expression levels, as well as its inhibition mechanisms. Each ce...
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| Veröffentlicht in: | Experimental and therapeutic medicine 2017-08, Vol.14 (2), p.1809-1817 |
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| creator | Sun, Yonghao Zhang, Dejuan Mao, Mao Lu, Yangping Jiao, Ning |
| description | The aim of the present study was to investigate the inhibitory effect of compound cantharides capsules (CCCs) on the viability and apoptosis of human gastric cancer cell lines, BGC-823 and SGC-7901, and to detect its regulation of gene expression levels, as well as its inhibition mechanisms. Each cell line was grouped into a control group, CCC serum group, 5-fluorouracil (5-FU) group, combination therapy group (CCC serum + 5-FU) and serum control group. Growth curves were measured and flow cytometry was used to detect cell apoptosis and cell viability. The mRNA expression level of proliferation-related C-MYC and p53 genes were assayed by reverse transcription-quantitative polymerase chain reaction. Protein phosphorylation levels of proliferating cell nuclear antigen, p38 mitogen-activated protein kinase, extracellular signal-related kinase 1/2, c-Jun N-terminal kinase (JNK) and IκB were assayed by western blotting. The combined CCC serum and 5-FU group exhibited a higher inhibition rate in both cell lines and CCC serum therapy demonstrated a similar effect to 5-FU treatment, as demonstrated in the MTT and cell growth assay. Combined therapy significantly decreased the C-MYC mRNA expression levels and increased p53 mRNA expression levels (P |
| doi_str_mv | 10.3892/etm.2017.4704 |
| format | Article |
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Each cell line was grouped into a control group, CCC serum group, 5-fluorouracil (5-FU) group, combination therapy group (CCC serum + 5-FU) and serum control group. Growth curves were measured and flow cytometry was used to detect cell apoptosis and cell viability. The mRNA expression level of proliferation-related C-MYC and p53 genes were assayed by reverse transcription-quantitative polymerase chain reaction. Protein phosphorylation levels of proliferating cell nuclear antigen, p38 mitogen-activated protein kinase, extracellular signal-related kinase 1/2, c-Jun N-terminal kinase (JNK) and IκB were assayed by western blotting. The combined CCC serum and 5-FU group exhibited a higher inhibition rate in both cell lines and CCC serum therapy demonstrated a similar effect to 5-FU treatment, as demonstrated in the MTT and cell growth assay. Combined therapy significantly decreased the C-MYC mRNA expression levels and increased p53 mRNA expression levels (P<0.05). Combined therapy of 5-FU and CCC was more significant compared with CCC serum or 5-FU only (P<0.05). P38 and JNK-related protein phosphorylation are involved in apoptosis initiated by CCC combined 5-FU therapy. Combined therapy was able to significantly inhibit human gastric cancer cell growth (P<0.05), and advance cell apoptosis compared with CCC serum only. CCC serum resulted in downregulation of the c-Myc gene and upregulation of the p53 gene. p38 and JNK-related protein phosphorylation is involved in the inhibition of cell viability and apoptosis of human gastric cancer cell lines.</description><identifier>ISSN: 1792-0981</identifier><identifier>EISSN: 1792-1015</identifier><identifier>DOI: 10.3892/etm.2017.4704</identifier><identifier>PMID: 28810654</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>5-fluorouracil ; Apoptosis ; c-Jun N-terminal kinase ; Cancer therapies ; cantharidin ; Cell culture ; Cell cycle ; Cell growth ; Chemotherapy ; Chinese medicine ; Cytochrome ; Drug dosages ; Gastric cancer ; gastric cancer cell ; Gene expression ; Kinases ; Liver cancer ; Lung cancer ; Lymphoma ; Medical research ; p38 ; Phosphorylation ; Proteins ; Rodents ; Tumors ; viability</subject><ispartof>Experimental and therapeutic medicine, 2017-08, Vol.14 (2), p.1809-1817</ispartof><rights>Copyright © 2017, Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2017</rights><rights>Copyright © 2017, Spandidos Publications 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-a15c50651834663d9721c783cd7d425b837125fe8d818dc94036d8f5a0678bbb3</citedby><cites>FETCH-LOGICAL-c445t-a15c50651834663d9721c783cd7d425b837125fe8d818dc94036d8f5a0678bbb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5526170/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5526170/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28810654$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Yonghao</creatorcontrib><creatorcontrib>Zhang, Dejuan</creatorcontrib><creatorcontrib>Mao, Mao</creatorcontrib><creatorcontrib>Lu, Yangping</creatorcontrib><creatorcontrib>Jiao, Ning</creatorcontrib><title>Roles of p38 and JNK protein kinase pathways activated by compound cantharidin capsules containing serum on proliferation inhibition and apoptosis of human gastric cancer cell line</title><title>Experimental and therapeutic medicine</title><addtitle>Exp Ther Med</addtitle><description>The aim of the present study was to investigate the inhibitory effect of compound cantharides capsules (CCCs) on the viability and apoptosis of human gastric cancer cell lines, BGC-823 and SGC-7901, and to detect its regulation of gene expression levels, as well as its inhibition mechanisms. Each cell line was grouped into a control group, CCC serum group, 5-fluorouracil (5-FU) group, combination therapy group (CCC serum + 5-FU) and serum control group. Growth curves were measured and flow cytometry was used to detect cell apoptosis and cell viability. The mRNA expression level of proliferation-related C-MYC and p53 genes were assayed by reverse transcription-quantitative polymerase chain reaction. Protein phosphorylation levels of proliferating cell nuclear antigen, p38 mitogen-activated protein kinase, extracellular signal-related kinase 1/2, c-Jun N-terminal kinase (JNK) and IκB were assayed by western blotting. The combined CCC serum and 5-FU group exhibited a higher inhibition rate in both cell lines and CCC serum therapy demonstrated a similar effect to 5-FU treatment, as demonstrated in the MTT and cell growth assay. Combined therapy significantly decreased the C-MYC mRNA expression levels and increased p53 mRNA expression levels (P<0.05). Combined therapy of 5-FU and CCC was more significant compared with CCC serum or 5-FU only (P<0.05). P38 and JNK-related protein phosphorylation are involved in apoptosis initiated by CCC combined 5-FU therapy. Combined therapy was able to significantly inhibit human gastric cancer cell growth (P<0.05), and advance cell apoptosis compared with CCC serum only. CCC serum resulted in downregulation of the c-Myc gene and upregulation of the p53 gene. p38 and JNK-related protein phosphorylation is involved in the inhibition of cell viability and apoptosis of human gastric cancer cell lines.</description><subject>5-fluorouracil</subject><subject>Apoptosis</subject><subject>c-Jun N-terminal kinase</subject><subject>Cancer therapies</subject><subject>cantharidin</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Chemotherapy</subject><subject>Chinese medicine</subject><subject>Cytochrome</subject><subject>Drug dosages</subject><subject>Gastric cancer</subject><subject>gastric cancer cell</subject><subject>Gene expression</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>Lung cancer</subject><subject>Lymphoma</subject><subject>Medical research</subject><subject>p38</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Tumors</subject><subject>viability</subject><issn>1792-0981</issn><issn>1792-1015</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpdksFu1DAQhiMEolXpkSuyhJC4ZLGdOLEvSKgqFCggoXK2Jraz65LYqe0U7Xv1AXF2lxVgHzyWv_lnRv6L4jnBq4oL-sakcUUxaVd1i-tHxSlpBS0JJuzxIcaCk5PiPMZbnBdrCOfsaXFCOSe4YfVp8fDdDyYi36Op4gicRp--fkZT8MlYh35aB9GgCdLmF2wjApXsPSSjUbdFyo-Tn3OGApc2EKzOGQqmOC-KyrsE1lm3RtGEeUTeLbKD7U2AZPPNuo3t7C5c6sLkp-Sj3TWzmUdwaA0xBauWAsoEpMwwoME686x40sMQzfnhPCt-vL-8ubgqr799-Hjx7rpUdc1SCYQplsckvKqbptKipUS1vFK61TVlHa9aQllvuOaEayVqXDWa9wxw0_Ku66qz4u1ed5q70WhlXAowyCnYEcJWerDy3xdnN3Lt7yVjtCEtzgKvDwLB380mJjnauIwBzvg5SiKoEBhTQjP68j_01s_B5fEyJWrBKt7WmSr3lAo-xmD6YzMEy8USMltCLpaQiyUy_-LvCY70HwNk4NUeiFP-BKt9PDKXN19KnPdO6DfP2MHg</recordid><startdate>20170801</startdate><enddate>20170801</enddate><creator>Sun, Yonghao</creator><creator>Zhang, Dejuan</creator><creator>Mao, Mao</creator><creator>Lu, Yangping</creator><creator>Jiao, Ning</creator><general>D.A. Spandidos</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170801</creationdate><title>Roles of p38 and JNK protein kinase pathways activated by compound cantharidin capsules containing serum on proliferation inhibition and apoptosis of human gastric cancer cell line</title><author>Sun, Yonghao ; Zhang, Dejuan ; Mao, Mao ; Lu, Yangping ; Jiao, Ning</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-a15c50651834663d9721c783cd7d425b837125fe8d818dc94036d8f5a0678bbb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>5-fluorouracil</topic><topic>Apoptosis</topic><topic>c-Jun N-terminal kinase</topic><topic>Cancer therapies</topic><topic>cantharidin</topic><topic>Cell culture</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Chemotherapy</topic><topic>Chinese medicine</topic><topic>Cytochrome</topic><topic>Drug dosages</topic><topic>Gastric cancer</topic><topic>gastric cancer cell</topic><topic>Gene expression</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>Lung cancer</topic><topic>Lymphoma</topic><topic>Medical research</topic><topic>p38</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Tumors</topic><topic>viability</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sun, Yonghao</creatorcontrib><creatorcontrib>Zhang, Dejuan</creatorcontrib><creatorcontrib>Mao, Mao</creatorcontrib><creatorcontrib>Lu, Yangping</creatorcontrib><creatorcontrib>Jiao, Ning</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Experimental and therapeutic medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Yonghao</au><au>Zhang, Dejuan</au><au>Mao, Mao</au><au>Lu, Yangping</au><au>Jiao, Ning</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Roles of p38 and JNK protein kinase pathways activated by compound cantharidin capsules containing serum on proliferation inhibition and apoptosis of human gastric cancer cell line</atitle><jtitle>Experimental and therapeutic medicine</jtitle><addtitle>Exp Ther Med</addtitle><date>2017-08-01</date><risdate>2017</risdate><volume>14</volume><issue>2</issue><spage>1809</spage><epage>1817</epage><pages>1809-1817</pages><issn>1792-0981</issn><eissn>1792-1015</eissn><abstract>The aim of the present study was to investigate the inhibitory effect of compound cantharides capsules (CCCs) on the viability and apoptosis of human gastric cancer cell lines, BGC-823 and SGC-7901, and to detect its regulation of gene expression levels, as well as its inhibition mechanisms. Each cell line was grouped into a control group, CCC serum group, 5-fluorouracil (5-FU) group, combination therapy group (CCC serum + 5-FU) and serum control group. Growth curves were measured and flow cytometry was used to detect cell apoptosis and cell viability. The mRNA expression level of proliferation-related C-MYC and p53 genes were assayed by reverse transcription-quantitative polymerase chain reaction. Protein phosphorylation levels of proliferating cell nuclear antigen, p38 mitogen-activated protein kinase, extracellular signal-related kinase 1/2, c-Jun N-terminal kinase (JNK) and IκB were assayed by western blotting. The combined CCC serum and 5-FU group exhibited a higher inhibition rate in both cell lines and CCC serum therapy demonstrated a similar effect to 5-FU treatment, as demonstrated in the MTT and cell growth assay. Combined therapy significantly decreased the C-MYC mRNA expression levels and increased p53 mRNA expression levels (P<0.05). Combined therapy of 5-FU and CCC was more significant compared with CCC serum or 5-FU only (P<0.05). P38 and JNK-related protein phosphorylation are involved in apoptosis initiated by CCC combined 5-FU therapy. Combined therapy was able to significantly inhibit human gastric cancer cell growth (P<0.05), and advance cell apoptosis compared with CCC serum only. CCC serum resulted in downregulation of the c-Myc gene and upregulation of the p53 gene. p38 and JNK-related protein phosphorylation is involved in the inhibition of cell viability and apoptosis of human gastric cancer cell lines.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>28810654</pmid><doi>10.3892/etm.2017.4704</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 5-fluorouracil Apoptosis c-Jun N-terminal kinase Cancer therapies cantharidin Cell culture Cell cycle Cell growth Chemotherapy Chinese medicine Cytochrome Drug dosages Gastric cancer gastric cancer cell Gene expression Kinases Liver cancer Lung cancer Lymphoma Medical research p38 Phosphorylation Proteins Rodents Tumors viability |
| title | Roles of p38 and JNK protein kinase pathways activated by compound cantharidin capsules containing serum on proliferation inhibition and apoptosis of human gastric cancer cell line |
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