14-3-3sigma-dependent resistance to cisplatin
A major factor that impedes the clinical success of cisplatin-based chemotherapy for cancer is cisplatin resistance by cancer cells. The sensitivity of parental HCT116 human colon cancer cell line and its isogenic gene-knockout sub-lines to cisplatin was determined by clonogenicity assay; furthermor...
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| Veröffentlicht in: | Anticancer research 2009-06, Vol.29 (6), p.2009-2014 |
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| container_title | Anticancer research |
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| creator | Han, Zhiyong Dimas, Konstantinos Tian, Xuefei Wang, Yongbao Hemmi, Hiromichi Yamada, Kanae Kato, Naoyuki Pantazis, Panayotis Ramanujam, Rama J Anant, Shrikant Wyche, James H Houchen, Courtney W |
| description | A major factor that impedes the clinical success of cisplatin-based chemotherapy for cancer is cisplatin resistance by cancer cells.
The sensitivity of parental HCT116 human colon cancer cell line and its isogenic gene-knockout sub-lines to cisplatin was determined by clonogenicity assay; furthermore, p53 activation, p21 expression, cell cycle arrest and senescence in these cells after cisplatin treatment were investigated.
Parental cells were six times more resistant than 14-3-3sigma-knockout (sigma-KO) cells to cisplatin. Moreover, activation of p53, p53-dependent expression of p21 and p21-dependent senescence were observed in sigma-KO, but not parental cells after a treatment with a low cisplatin dose.
A 14-3-3sigma-dependent mechanism inhibits p53 activation in parental cells treated with a low cisplatin dose, thereby blocking p21 expression that is essential for senescence and consequently conferring to the parental cells a significant degree of resistance to cisplatin. |
| format | Article |
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The sensitivity of parental HCT116 human colon cancer cell line and its isogenic gene-knockout sub-lines to cisplatin was determined by clonogenicity assay; furthermore, p53 activation, p21 expression, cell cycle arrest and senescence in these cells after cisplatin treatment were investigated.
Parental cells were six times more resistant than 14-3-3sigma-knockout (sigma-KO) cells to cisplatin. Moreover, activation of p53, p53-dependent expression of p21 and p21-dependent senescence were observed in sigma-KO, but not parental cells after a treatment with a low cisplatin dose.
A 14-3-3sigma-dependent mechanism inhibits p53 activation in parental cells treated with a low cisplatin dose, thereby blocking p21 expression that is essential for senescence and consequently conferring to the parental cells a significant degree of resistance to cisplatin.</description><identifier>ISSN: 0250-7005</identifier><identifier>PMID: 19528459</identifier><language>eng</language><publisher>Greece</publisher><subject>14-3-3 Proteins ; Antineoplastic Agents - pharmacology ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Blotting, Western ; Cellular Senescence - drug effects ; Cisplatin - pharmacology ; Colonic Neoplasms - drug therapy ; Colonic Neoplasms - metabolism ; Colonic Neoplasms - pathology ; Cyclin-Dependent Kinase Inhibitor p21 - physiology ; Drug Resistance, Neoplasm ; Exonucleases - genetics ; Exonucleases - metabolism ; Exoribonucleases ; Flow Cytometry ; Gene Knockout Techniques ; Humans ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Tumor Cells, Cultured ; Tumor Stem Cell Assay ; Tumor Suppressor Protein p53 - physiology</subject><ispartof>Anticancer research, 2009-06, Vol.29 (6), p.2009-2014</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19528459$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Han, Zhiyong</creatorcontrib><creatorcontrib>Dimas, Konstantinos</creatorcontrib><creatorcontrib>Tian, Xuefei</creatorcontrib><creatorcontrib>Wang, Yongbao</creatorcontrib><creatorcontrib>Hemmi, Hiromichi</creatorcontrib><creatorcontrib>Yamada, Kanae</creatorcontrib><creatorcontrib>Kato, Naoyuki</creatorcontrib><creatorcontrib>Pantazis, Panayotis</creatorcontrib><creatorcontrib>Ramanujam, Rama J</creatorcontrib><creatorcontrib>Anant, Shrikant</creatorcontrib><creatorcontrib>Wyche, James H</creatorcontrib><creatorcontrib>Houchen, Courtney W</creatorcontrib><title>14-3-3sigma-dependent resistance to cisplatin</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>A major factor that impedes the clinical success of cisplatin-based chemotherapy for cancer is cisplatin resistance by cancer cells.
The sensitivity of parental HCT116 human colon cancer cell line and its isogenic gene-knockout sub-lines to cisplatin was determined by clonogenicity assay; furthermore, p53 activation, p21 expression, cell cycle arrest and senescence in these cells after cisplatin treatment were investigated.
Parental cells were six times more resistant than 14-3-3sigma-knockout (sigma-KO) cells to cisplatin. Moreover, activation of p53, p53-dependent expression of p21 and p21-dependent senescence were observed in sigma-KO, but not parental cells after a treatment with a low cisplatin dose.
A 14-3-3sigma-dependent mechanism inhibits p53 activation in parental cells treated with a low cisplatin dose, thereby blocking p21 expression that is essential for senescence and consequently conferring to the parental cells a significant degree of resistance to cisplatin.</description><subject>14-3-3 Proteins</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Blotting, Western</subject><subject>Cellular Senescence - drug effects</subject><subject>Cisplatin - pharmacology</subject><subject>Colonic Neoplasms - drug therapy</subject><subject>Colonic Neoplasms - metabolism</subject><subject>Colonic Neoplasms - pathology</subject><subject>Cyclin-Dependent Kinase Inhibitor p21 - physiology</subject><subject>Drug Resistance, Neoplasm</subject><subject>Exonucleases - genetics</subject><subject>Exonucleases - metabolism</subject><subject>Exoribonucleases</subject><subject>Flow Cytometry</subject><subject>Gene Knockout Techniques</subject><subject>Humans</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Stem Cell Assay</subject><subject>Tumor Suppressor Protein p53 - physiology</subject><issn>0250-7005</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1j7tqwzAUQDW0NGmaXyieuglkXUnWHUvoCwJZshtZugoqfqiWPfTvW2g6neVw4NywrZBa8EYIvWH3pXwKYQxauGObGrW0SuOW8Vpx4FDSZXA8UKYx0LhUM5VUFjd6qpap8qnk3i1pfGC30fWF9lfu2Pn15Xx458fT28fh-cizVsi17HSnJQAKK30d0SBBDCo0BJ3rhEOwjQ8ukiGjrI01og6ghfKE0ljYsae_bJ6nr5XK0g6peOp7N9K0ltY00KAE8ys-XsW1Gyi0eU6Dm7_b_z_4AZ5LSVk</recordid><startdate>200906</startdate><enddate>200906</enddate><creator>Han, Zhiyong</creator><creator>Dimas, Konstantinos</creator><creator>Tian, Xuefei</creator><creator>Wang, Yongbao</creator><creator>Hemmi, Hiromichi</creator><creator>Yamada, Kanae</creator><creator>Kato, Naoyuki</creator><creator>Pantazis, Panayotis</creator><creator>Ramanujam, Rama J</creator><creator>Anant, Shrikant</creator><creator>Wyche, James H</creator><creator>Houchen, Courtney W</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200906</creationdate><title>14-3-3sigma-dependent resistance to cisplatin</title><author>Han, Zhiyong ; 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The sensitivity of parental HCT116 human colon cancer cell line and its isogenic gene-knockout sub-lines to cisplatin was determined by clonogenicity assay; furthermore, p53 activation, p21 expression, cell cycle arrest and senescence in these cells after cisplatin treatment were investigated.
Parental cells were six times more resistant than 14-3-3sigma-knockout (sigma-KO) cells to cisplatin. Moreover, activation of p53, p53-dependent expression of p21 and p21-dependent senescence were observed in sigma-KO, but not parental cells after a treatment with a low cisplatin dose.
A 14-3-3sigma-dependent mechanism inhibits p53 activation in parental cells treated with a low cisplatin dose, thereby blocking p21 expression that is essential for senescence and consequently conferring to the parental cells a significant degree of resistance to cisplatin.</abstract><cop>Greece</cop><pmid>19528459</pmid><tpages>6</tpages></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | 14-3-3 Proteins Antineoplastic Agents - pharmacology Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Blotting, Western Cellular Senescence - drug effects Cisplatin - pharmacology Colonic Neoplasms - drug therapy Colonic Neoplasms - metabolism Colonic Neoplasms - pathology Cyclin-Dependent Kinase Inhibitor p21 - physiology Drug Resistance, Neoplasm Exonucleases - genetics Exonucleases - metabolism Exoribonucleases Flow Cytometry Gene Knockout Techniques Humans Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Tumor Cells, Cultured Tumor Stem Cell Assay Tumor Suppressor Protein p53 - physiology |
| title | 14-3-3sigma-dependent resistance to cisplatin |
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