Synergistic cytotoxicity of the dipeptidyl peptidase-IV inhibitor gemigliptin with metformin in thyroid carcinoma cells
Purpose The influence of the dipeptidyl peptidase-IV inhibitor, gemigliptin alone or in combination with metformin on survival, proliferation, and migration of thyroid carcinoma cells was investigated. Methods SW1736 and TPC-1 human thyroid carcinoma cells were used. Results Gemigliptin and metformi...
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| Veröffentlicht in: | Endocrine 2018-02, Vol.59 (2), p.383-394 |
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| creator | Kim, Si Hyoung Kang, Jun Goo Kim, Chul Sik Ihm, Sung-Hee Choi, Moon Gi Yoo, Hyung Joon Lee, Seong Jin |
| description | Purpose
The influence of the dipeptidyl peptidase-IV inhibitor, gemigliptin alone or in combination with metformin on survival, proliferation, and migration of thyroid carcinoma cells was investigated.
Methods
SW1736 and TPC-1 human thyroid carcinoma cells were used.
Results
Gemigliptin and metformin caused cell death in a dose-dependent manner. In cells treated with both gemigliptin and metformin, compared with metformin alone, all of the combination index values were lower than 1.0, suggesting synergistic cytotoxicity of two agents. Cell viability, the percentage of viable cells, ATP levels, and mitochondrial membrane potential decreased; however, cytotoxic activity, and the protein levels of cleaved PARP, phospho-Akt and phospho-AMP-activated protein kinase (AMPK) increased. Administration of wortmannin, but not compound C, further decreased cell viability, and further increased cytotoxic activity. Moreover, compared with control, cell proliferation and migration as well as the protein levels of p53, p21, vascular cell adhesion molecule-1 (VCAM-1), and phospho-extracellular signal-regulated kinase (ERK) 1/2 decreased. The decrement of matrix metalloproteinase-2 and matrix metalloproteinase-9 protein levels was cell specific.
Conclusions
Our results demonstrate that gemigliptin induces cytotoxic activity, and has a synergistic activity with metformin in inducing cytotoxicity via regulation of Akt and AMPK in thyroid carcinoma cells. Furthermore, gemigliptin augments the inhibitory effect of metformin on proliferation and migration through involvement of matrix metalloproteinase-2, matrix metalloproteinase-9, p53, p21, VCAM-1, and ERK in thyroid carcinoma cells. |
| doi_str_mv | 10.1007/s12020-017-1503-2 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1982841124</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1993040292</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-2b0bbfce33226b348088a582a301e1ce981a499eb1239a1b58c36297467484353</originalsourceid><addsrcrecordid>eNp1kV9rHCEUxaUkNGnaD9CXIPSlL9NcddzRxxKSNhDIQ_7QN3HcO7uGmXGrLtv59nGZJIRCQPDq_d3jwUPIVwY_GEBzlhgHDhWwpmISRMU_kGMmpS43AAelFlJWAOrPEfmU0iMA53zRfCRHXHMlFxKOye52GjGufMreUTflkMM_73yeaOhoXiNd-g1usl9OPZ0Lm7C6eqB-XPvW5xDpCge_6n3pjXTn85oOmLsQh3IsK6-nGPySOhudH8NgqcO-T5_JYWf7hF-e9xNyf3lxd_67ur75dXX-87pyouG54i20bedQiOK8FbUCpaxU3ApgyBxqxWytNbaMC21ZK5UTC66betHUqhZSnJDvs-4mhr9bTNkMPu0d2BHDNhmmFVc1Y7wu6Lf_0MewjWNxVygtoIbybYViM-ViSCliZzbRDzZOhoHZp2LmVExJxexTMfuZ02flbTvg8nXiJYYC8BlIpTWuML55-l3VJ-9mmEY</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1993040292</pqid></control><display><type>article</type><title>Synergistic cytotoxicity of the dipeptidyl peptidase-IV inhibitor gemigliptin with metformin in thyroid carcinoma cells</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Kim, Si Hyoung ; Kang, Jun Goo ; Kim, Chul Sik ; Ihm, Sung-Hee ; Choi, Moon Gi ; Yoo, Hyung Joon ; Lee, Seong Jin</creator><creatorcontrib>Kim, Si Hyoung ; Kang, Jun Goo ; Kim, Chul Sik ; Ihm, Sung-Hee ; Choi, Moon Gi ; Yoo, Hyung Joon ; Lee, Seong Jin</creatorcontrib><description>Purpose
The influence of the dipeptidyl peptidase-IV inhibitor, gemigliptin alone or in combination with metformin on survival, proliferation, and migration of thyroid carcinoma cells was investigated.
Methods
SW1736 and TPC-1 human thyroid carcinoma cells were used.
Results
Gemigliptin and metformin caused cell death in a dose-dependent manner. In cells treated with both gemigliptin and metformin, compared with metformin alone, all of the combination index values were lower than 1.0, suggesting synergistic cytotoxicity of two agents. Cell viability, the percentage of viable cells, ATP levels, and mitochondrial membrane potential decreased; however, cytotoxic activity, and the protein levels of cleaved PARP, phospho-Akt and phospho-AMP-activated protein kinase (AMPK) increased. Administration of wortmannin, but not compound C, further decreased cell viability, and further increased cytotoxic activity. Moreover, compared with control, cell proliferation and migration as well as the protein levels of p53, p21, vascular cell adhesion molecule-1 (VCAM-1), and phospho-extracellular signal-regulated kinase (ERK) 1/2 decreased. The decrement of matrix metalloproteinase-2 and matrix metalloproteinase-9 protein levels was cell specific.
Conclusions
Our results demonstrate that gemigliptin induces cytotoxic activity, and has a synergistic activity with metformin in inducing cytotoxicity via regulation of Akt and AMPK in thyroid carcinoma cells. Furthermore, gemigliptin augments the inhibitory effect of metformin on proliferation and migration through involvement of matrix metalloproteinase-2, matrix metalloproteinase-9, p53, p21, VCAM-1, and ERK in thyroid carcinoma cells.</description><identifier>ISSN: 1355-008X</identifier><identifier>EISSN: 1559-0100</identifier><identifier>DOI: 10.1007/s12020-017-1503-2</identifier><identifier>PMID: 29285650</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>AKT protein ; AMP ; AMP-activated protein kinase ; AMP-Activated Protein Kinases - metabolism ; Cell adhesion & migration ; Cell adhesion molecules ; Cell death ; Cell Death - drug effects ; Cell Line, Tumor ; Cell migration ; Cell Movement - drug effects ; Cell proliferation ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cyclin-dependent kinase inhibitor p21 ; Cytotoxicity ; Diabetes ; Dipeptidyl-peptidase IV ; Dipeptidyl-Peptidase IV Inhibitors - pharmacology ; Dipeptidyl-Peptidase IV Inhibitors - therapeutic use ; Dose-Response Relationship, Drug ; Drug Synergism ; Endocrinology ; Extracellular signal-regulated kinase ; GTP-binding protein ; Humanities and Social Sciences ; Humans ; Hypoglycemic Agents - pharmacology ; Hypoglycemic Agents - therapeutic use ; Internal Medicine ; Kinases ; Matrix metalloproteinase ; Matrix Metalloproteinase 2 - metabolism ; Matrix Metalloproteinase 9 - metabolism ; Medicine ; Medicine & Public Health ; Membrane potential ; Membrane Potential, Mitochondrial - drug effects ; Metalloproteinase ; Metformin ; Metformin - pharmacology ; Metformin - therapeutic use ; Mitochondria ; multidisciplinary ; Original Article ; p53 Protein ; Peptidase ; Phosphorylation - drug effects ; Piperidones - pharmacology ; Piperidones - therapeutic use ; Poly(ADP-ribose) polymerase ; Proteins ; Pyrimidines - pharmacology ; Pyrimidines - therapeutic use ; Science ; Signal Transduction - drug effects ; Thyroid cancer ; Thyroid carcinoma ; Thyroid Neoplasms - drug therapy ; Thyroid Neoplasms - metabolism ; Thyroid Neoplasms - pathology ; Vascular cell adhesion molecule 1 ; Vascular Cell Adhesion Molecule-1 - metabolism ; Wortmannin</subject><ispartof>Endocrine, 2018-02, Vol.59 (2), p.383-394</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2017</rights><rights>Copyright Springer Science & Business Media 2018</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-2b0bbfce33226b348088a582a301e1ce981a499eb1239a1b58c36297467484353</citedby><cites>FETCH-LOGICAL-c372t-2b0bbfce33226b348088a582a301e1ce981a499eb1239a1b58c36297467484353</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/s12020-017-1503-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12020-017-1503-2$$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/29285650$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Si Hyoung</creatorcontrib><creatorcontrib>Kang, Jun Goo</creatorcontrib><creatorcontrib>Kim, Chul Sik</creatorcontrib><creatorcontrib>Ihm, Sung-Hee</creatorcontrib><creatorcontrib>Choi, Moon Gi</creatorcontrib><creatorcontrib>Yoo, Hyung Joon</creatorcontrib><creatorcontrib>Lee, Seong Jin</creatorcontrib><title>Synergistic cytotoxicity of the dipeptidyl peptidase-IV inhibitor gemigliptin with metformin in thyroid carcinoma cells</title><title>Endocrine</title><addtitle>Endocrine</addtitle><addtitle>Endocrine</addtitle><description>Purpose
The influence of the dipeptidyl peptidase-IV inhibitor, gemigliptin alone or in combination with metformin on survival, proliferation, and migration of thyroid carcinoma cells was investigated.
Methods
SW1736 and TPC-1 human thyroid carcinoma cells were used.
Results
Gemigliptin and metformin caused cell death in a dose-dependent manner. In cells treated with both gemigliptin and metformin, compared with metformin alone, all of the combination index values were lower than 1.0, suggesting synergistic cytotoxicity of two agents. Cell viability, the percentage of viable cells, ATP levels, and mitochondrial membrane potential decreased; however, cytotoxic activity, and the protein levels of cleaved PARP, phospho-Akt and phospho-AMP-activated protein kinase (AMPK) increased. Administration of wortmannin, but not compound C, further decreased cell viability, and further increased cytotoxic activity. Moreover, compared with control, cell proliferation and migration as well as the protein levels of p53, p21, vascular cell adhesion molecule-1 (VCAM-1), and phospho-extracellular signal-regulated kinase (ERK) 1/2 decreased. The decrement of matrix metalloproteinase-2 and matrix metalloproteinase-9 protein levels was cell specific.
Conclusions
Our results demonstrate that gemigliptin induces cytotoxic activity, and has a synergistic activity with metformin in inducing cytotoxicity via regulation of Akt and AMPK in thyroid carcinoma cells. Furthermore, gemigliptin augments the inhibitory effect of metformin on proliferation and migration through involvement of matrix metalloproteinase-2, matrix metalloproteinase-9, p53, p21, VCAM-1, and ERK in thyroid carcinoma cells.</description><subject>AKT protein</subject><subject>AMP</subject><subject>AMP-activated protein kinase</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Cell adhesion & migration</subject><subject>Cell adhesion molecules</subject><subject>Cell death</subject><subject>Cell Death - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cyclin-dependent kinase inhibitor p21</subject><subject>Cytotoxicity</subject><subject>Diabetes</subject><subject>Dipeptidyl-peptidase IV</subject><subject>Dipeptidyl-Peptidase IV Inhibitors - pharmacology</subject><subject>Dipeptidyl-Peptidase IV Inhibitors - therapeutic use</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Synergism</subject><subject>Endocrinology</subject><subject>Extracellular signal-regulated kinase</subject><subject>GTP-binding protein</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Internal Medicine</subject><subject>Kinases</subject><subject>Matrix metalloproteinase</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Membrane potential</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Metalloproteinase</subject><subject>Metformin</subject><subject>Metformin - pharmacology</subject><subject>Metformin - therapeutic use</subject><subject>Mitochondria</subject><subject>multidisciplinary</subject><subject>Original Article</subject><subject>p53 Protein</subject><subject>Peptidase</subject><subject>Phosphorylation - drug effects</subject><subject>Piperidones - pharmacology</subject><subject>Piperidones - therapeutic use</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Proteins</subject><subject>Pyrimidines - pharmacology</subject><subject>Pyrimidines - therapeutic use</subject><subject>Science</subject><subject>Signal Transduction - drug effects</subject><subject>Thyroid cancer</subject><subject>Thyroid carcinoma</subject><subject>Thyroid Neoplasms - drug therapy</subject><subject>Thyroid Neoplasms - metabolism</subject><subject>Thyroid Neoplasms - pathology</subject><subject>Vascular cell adhesion molecule 1</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><subject>Wortmannin</subject><issn>1355-008X</issn><issn>1559-0100</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kV9rHCEUxaUkNGnaD9CXIPSlL9NcddzRxxKSNhDIQ_7QN3HcO7uGmXGrLtv59nGZJIRCQPDq_d3jwUPIVwY_GEBzlhgHDhWwpmISRMU_kGMmpS43AAelFlJWAOrPEfmU0iMA53zRfCRHXHMlFxKOye52GjGufMreUTflkMM_73yeaOhoXiNd-g1usl9OPZ0Lm7C6eqB-XPvW5xDpCge_6n3pjXTn85oOmLsQh3IsK6-nGPySOhudH8NgqcO-T5_JYWf7hF-e9xNyf3lxd_67ur75dXX-87pyouG54i20bedQiOK8FbUCpaxU3ApgyBxqxWytNbaMC21ZK5UTC66betHUqhZSnJDvs-4mhr9bTNkMPu0d2BHDNhmmFVc1Y7wu6Lf_0MewjWNxVygtoIbybYViM-ViSCliZzbRDzZOhoHZp2LmVExJxexTMfuZ02flbTvg8nXiJYYC8BlIpTWuML55-l3VJ-9mmEY</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Kim, Si Hyoung</creator><creator>Kang, Jun Goo</creator><creator>Kim, Chul Sik</creator><creator>Ihm, Sung-Hee</creator><creator>Choi, Moon Gi</creator><creator>Yoo, Hyung Joon</creator><creator>Lee, Seong Jin</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>7X8</scope></search><sort><creationdate>20180201</creationdate><title>Synergistic cytotoxicity of the dipeptidyl peptidase-IV inhibitor gemigliptin with metformin in thyroid carcinoma cells</title><author>Kim, Si Hyoung ; Kang, Jun Goo ; Kim, Chul Sik ; Ihm, Sung-Hee ; Choi, Moon Gi ; Yoo, Hyung Joon ; Lee, Seong Jin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-2b0bbfce33226b348088a582a301e1ce981a499eb1239a1b58c36297467484353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>AKT protein</topic><topic>AMP</topic><topic>AMP-activated protein kinase</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Cell adhesion & migration</topic><topic>Cell adhesion molecules</topic><topic>Cell death</topic><topic>Cell Death - drug effects</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cyclin-dependent kinase inhibitor p21</topic><topic>Cytotoxicity</topic><topic>Diabetes</topic><topic>Dipeptidyl-peptidase IV</topic><topic>Dipeptidyl-Peptidase IV Inhibitors - pharmacology</topic><topic>Dipeptidyl-Peptidase IV Inhibitors - therapeutic use</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Synergism</topic><topic>Endocrinology</topic><topic>Extracellular signal-regulated kinase</topic><topic>GTP-binding protein</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Internal Medicine</topic><topic>Kinases</topic><topic>Matrix metalloproteinase</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Membrane potential</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Metalloproteinase</topic><topic>Metformin</topic><topic>Metformin - pharmacology</topic><topic>Metformin - therapeutic use</topic><topic>Mitochondria</topic><topic>multidisciplinary</topic><topic>Original Article</topic><topic>p53 Protein</topic><topic>Peptidase</topic><topic>Phosphorylation - drug effects</topic><topic>Piperidones - pharmacology</topic><topic>Piperidones - therapeutic use</topic><topic>Poly(ADP-ribose) polymerase</topic><topic>Proteins</topic><topic>Pyrimidines - pharmacology</topic><topic>Pyrimidines - therapeutic use</topic><topic>Science</topic><topic>Signal Transduction - drug effects</topic><topic>Thyroid cancer</topic><topic>Thyroid carcinoma</topic><topic>Thyroid Neoplasms - drug therapy</topic><topic>Thyroid Neoplasms - metabolism</topic><topic>Thyroid Neoplasms - pathology</topic><topic>Vascular cell adhesion molecule 1</topic><topic>Vascular Cell Adhesion Molecule-1 - metabolism</topic><topic>Wortmannin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Si Hyoung</creatorcontrib><creatorcontrib>Kang, Jun Goo</creatorcontrib><creatorcontrib>Kim, Chul Sik</creatorcontrib><creatorcontrib>Ihm, Sung-Hee</creatorcontrib><creatorcontrib>Choi, Moon Gi</creatorcontrib><creatorcontrib>Yoo, Hyung Joon</creatorcontrib><creatorcontrib>Lee, Seong Jin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Si Hyoung</au><au>Kang, Jun Goo</au><au>Kim, Chul Sik</au><au>Ihm, Sung-Hee</au><au>Choi, Moon Gi</au><au>Yoo, Hyung Joon</au><au>Lee, Seong Jin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Synergistic cytotoxicity of the dipeptidyl peptidase-IV inhibitor gemigliptin with metformin in thyroid carcinoma cells</atitle><jtitle>Endocrine</jtitle><stitle>Endocrine</stitle><addtitle>Endocrine</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>59</volume><issue>2</issue><spage>383</spage><epage>394</epage><pages>383-394</pages><issn>1355-008X</issn><eissn>1559-0100</eissn><abstract>Purpose
The influence of the dipeptidyl peptidase-IV inhibitor, gemigliptin alone or in combination with metformin on survival, proliferation, and migration of thyroid carcinoma cells was investigated.
Methods
SW1736 and TPC-1 human thyroid carcinoma cells were used.
Results
Gemigliptin and metformin caused cell death in a dose-dependent manner. In cells treated with both gemigliptin and metformin, compared with metformin alone, all of the combination index values were lower than 1.0, suggesting synergistic cytotoxicity of two agents. Cell viability, the percentage of viable cells, ATP levels, and mitochondrial membrane potential decreased; however, cytotoxic activity, and the protein levels of cleaved PARP, phospho-Akt and phospho-AMP-activated protein kinase (AMPK) increased. Administration of wortmannin, but not compound C, further decreased cell viability, and further increased cytotoxic activity. Moreover, compared with control, cell proliferation and migration as well as the protein levels of p53, p21, vascular cell adhesion molecule-1 (VCAM-1), and phospho-extracellular signal-regulated kinase (ERK) 1/2 decreased. The decrement of matrix metalloproteinase-2 and matrix metalloproteinase-9 protein levels was cell specific.
Conclusions
Our results demonstrate that gemigliptin induces cytotoxic activity, and has a synergistic activity with metformin in inducing cytotoxicity via regulation of Akt and AMPK in thyroid carcinoma cells. Furthermore, gemigliptin augments the inhibitory effect of metformin on proliferation and migration through involvement of matrix metalloproteinase-2, matrix metalloproteinase-9, p53, p21, VCAM-1, and ERK in thyroid carcinoma cells.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>29285650</pmid><doi>10.1007/s12020-017-1503-2</doi><tpages>12</tpages></addata></record> |
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| source | MEDLINE; SpringerNature Journals |
| subjects | AKT protein AMP AMP-activated protein kinase AMP-Activated Protein Kinases - metabolism Cell adhesion & migration Cell adhesion molecules Cell death Cell Death - drug effects Cell Line, Tumor Cell migration Cell Movement - drug effects Cell proliferation Cell Proliferation - drug effects Cell Survival - drug effects Cyclin-dependent kinase inhibitor p21 Cytotoxicity Diabetes Dipeptidyl-peptidase IV Dipeptidyl-Peptidase IV Inhibitors - pharmacology Dipeptidyl-Peptidase IV Inhibitors - therapeutic use Dose-Response Relationship, Drug Drug Synergism Endocrinology Extracellular signal-regulated kinase GTP-binding protein Humanities and Social Sciences Humans Hypoglycemic Agents - pharmacology Hypoglycemic Agents - therapeutic use Internal Medicine Kinases Matrix metalloproteinase Matrix Metalloproteinase 2 - metabolism Matrix Metalloproteinase 9 - metabolism Medicine Medicine & Public Health Membrane potential Membrane Potential, Mitochondrial - drug effects Metalloproteinase Metformin Metformin - pharmacology Metformin - therapeutic use Mitochondria multidisciplinary Original Article p53 Protein Peptidase Phosphorylation - drug effects Piperidones - pharmacology Piperidones - therapeutic use Poly(ADP-ribose) polymerase Proteins Pyrimidines - pharmacology Pyrimidines - therapeutic use Science Signal Transduction - drug effects Thyroid cancer Thyroid carcinoma Thyroid Neoplasms - drug therapy Thyroid Neoplasms - metabolism Thyroid Neoplasms - pathology Vascular cell adhesion molecule 1 Vascular Cell Adhesion Molecule-1 - metabolism Wortmannin |
| title | Synergistic cytotoxicity of the dipeptidyl peptidase-IV inhibitor gemigliptin with metformin in thyroid carcinoma cells |
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