The Suppression of Aurora-A/STK15/BTAK Expression Enhances Chemosensitivity to Docetaxel in Human Esophageal Squamous Cell Carcinoma
Purpose: We previously reported that the expression of Aurora-A was frequently up-regulated in human esophageal squamous cell carcinoma (ESCC) tissues as well as cell lines and the up-regulation contributed to a poor prognosis. In this study, we assessed the possibility of Aurora-A suppression as a...
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| Veröffentlicht in: | Clinical cancer research 2007-02, Vol.13 (4), p.1331-1340 |
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| creator | TANAKA, Eiji HASHIMOTO, Yosuke ITO, Tetsuo KONDO, Kan HIGASHIYAMA, Motoshige TSUNODA, Shigeru ORTIZ, Cristian SAKAI, Yoshiharu INAZAWA, Johji SHIMADA, Yutaka |
| description | Purpose: We previously reported that the expression of Aurora-A was frequently up-regulated in human esophageal squamous cell carcinoma
(ESCC) tissues as well as cell lines and the up-regulation contributed to a poor prognosis. In this study, we assessed the
possibility of Aurora-A suppression as a therapeutic target for ESCC using ESCC cell lines.
Experimental Design: We established subclones using vector-based short hairpin RNA (shRNA). Then, we investigated the effect of Aurora-A suppression
on proliferation and cell cycle changes in vitro . Next, chemosensitivity against docetaxel was investigated by tetrazolium salt–based proliferation assay (WST assay) and
cell number determinations, and furthermore, the type of cell death induced by docetaxel was analyzed by flow cytometry. Finally,
to examine the effect of Aurora-A shRNA on proliferation and chemosensitivity against docetaxel in vivo , a s.c. tumor formation assay in nude mice was done.
Results: We established two genetically different stable cell lines (510 A and 1440 A) in which levels of Aurora-A were reduced. Cell
growth was inhibited by 38.7% in 510 A and by 24.3% in 1440 A in vitro compared with empty vector–transfected controls (510 m and 1440 m), and this growth inhibition was mediated through G 2 -M arrest as confirmed by flow cytometry. Next, in a WST assay, the IC 50 for Aurora-A shRNA-transfected cells was lower than that of empty vector–transfected cells (510 A, 2.7 × 10 −7 mol/L; 510 m, 4.8 × 10 −7 mol/L; 1440 A, 2.6 × 10 −7 mol/L; 1440 m, 4.9 × 10 −7 mol/L). In addition, 0.3 nmol/L docetaxel induced a notable level of apoptosis in Aurora-A shRNA-transfected cells compared
with empty vector–transfected cells. In the assay of s.c. tumors in nude mice, tumor growth in 510 A was inhibited by 36.1%
compared with that in 510 m, and in tumors treated with docetaxel, the suppression of Aurora-A resulted in 44.0% tumor growth
suppression in vivo .
Conclusions: These results indicated that Aurora-A might play an important role in chemosensitivity to docetaxel, and the suppression
of its expression might be a potential therapeutic target for ESCC. |
| doi_str_mv | 10.1158/1078-0432.CCR-06-1192 |
| format | Article |
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(ESCC) tissues as well as cell lines and the up-regulation contributed to a poor prognosis. In this study, we assessed the
possibility of Aurora-A suppression as a therapeutic target for ESCC using ESCC cell lines.
Experimental Design: We established subclones using vector-based short hairpin RNA (shRNA). Then, we investigated the effect of Aurora-A suppression
on proliferation and cell cycle changes in vitro . Next, chemosensitivity against docetaxel was investigated by tetrazolium salt–based proliferation assay (WST assay) and
cell number determinations, and furthermore, the type of cell death induced by docetaxel was analyzed by flow cytometry. Finally,
to examine the effect of Aurora-A shRNA on proliferation and chemosensitivity against docetaxel in vivo , a s.c. tumor formation assay in nude mice was done.
Results: We established two genetically different stable cell lines (510 A and 1440 A) in which levels of Aurora-A were reduced. Cell
growth was inhibited by 38.7% in 510 A and by 24.3% in 1440 A in vitro compared with empty vector–transfected controls (510 m and 1440 m), and this growth inhibition was mediated through G 2 -M arrest as confirmed by flow cytometry. Next, in a WST assay, the IC 50 for Aurora-A shRNA-transfected cells was lower than that of empty vector–transfected cells (510 A, 2.7 × 10 −7 mol/L; 510 m, 4.8 × 10 −7 mol/L; 1440 A, 2.6 × 10 −7 mol/L; 1440 m, 4.9 × 10 −7 mol/L). In addition, 0.3 nmol/L docetaxel induced a notable level of apoptosis in Aurora-A shRNA-transfected cells compared
with empty vector–transfected cells. In the assay of s.c. tumors in nude mice, tumor growth in 510 A was inhibited by 36.1%
compared with that in 510 m, and in tumors treated with docetaxel, the suppression of Aurora-A resulted in 44.0% tumor growth
suppression in vivo .
Conclusions: These results indicated that Aurora-A might play an important role in chemosensitivity to docetaxel, and the suppression
of its expression might be a potential therapeutic target for ESCC.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-06-1192</identifier><identifier>PMID: 17317845</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Antineoplastic agents ; Antineoplastic Agents - pharmacology ; Aurora Kinase A ; Aurora Kinases ; Aurora-A ; Biological and medical sciences ; Carcinoma, Squamous Cell - drug therapy ; Carcinoma, Squamous Cell - enzymology ; Carcinoma, Squamous Cell - pathology ; Cell Line, Tumor ; chemosensitivity ; Esophageal Neoplasms - drug therapy ; Esophageal Neoplasms - enzymology ; Esophageal Neoplasms - pathology ; esophageal squamous cell carcinoma ; Esophagus ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Male ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Pharmacology. Drug treatments ; Protein-Serine-Threonine Kinases - antagonists & inhibitors ; Protein-Serine-Threonine Kinases - biosynthesis ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - metabolism ; RNA, Small Interfering - genetics ; shRNA ; Taxoids - metabolism ; Taxoids - pharmacology ; Tumors ; Xenograft Model Antitumor Assays</subject><ispartof>Clinical cancer research, 2007-02, Vol.13 (4), p.1331-1340</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c483t-7b2ec269320f4063fbbefb36489a2b4723be7a34888eb382bf4e0b68ae3892443</citedby><cites>FETCH-LOGICAL-c483t-7b2ec269320f4063fbbefb36489a2b4723be7a34888eb382bf4e0b68ae3892443</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3356,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18700037$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17317845$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>TANAKA, Eiji</creatorcontrib><creatorcontrib>HASHIMOTO, Yosuke</creatorcontrib><creatorcontrib>ITO, Tetsuo</creatorcontrib><creatorcontrib>KONDO, Kan</creatorcontrib><creatorcontrib>HIGASHIYAMA, Motoshige</creatorcontrib><creatorcontrib>TSUNODA, Shigeru</creatorcontrib><creatorcontrib>ORTIZ, Cristian</creatorcontrib><creatorcontrib>SAKAI, Yoshiharu</creatorcontrib><creatorcontrib>INAZAWA, Johji</creatorcontrib><creatorcontrib>SHIMADA, Yutaka</creatorcontrib><title>The Suppression of Aurora-A/STK15/BTAK Expression Enhances Chemosensitivity to Docetaxel in Human Esophageal Squamous Cell Carcinoma</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Purpose: We previously reported that the expression of Aurora-A was frequently up-regulated in human esophageal squamous cell carcinoma
(ESCC) tissues as well as cell lines and the up-regulation contributed to a poor prognosis. In this study, we assessed the
possibility of Aurora-A suppression as a therapeutic target for ESCC using ESCC cell lines.
Experimental Design: We established subclones using vector-based short hairpin RNA (shRNA). Then, we investigated the effect of Aurora-A suppression
on proliferation and cell cycle changes in vitro . Next, chemosensitivity against docetaxel was investigated by tetrazolium salt–based proliferation assay (WST assay) and
cell number determinations, and furthermore, the type of cell death induced by docetaxel was analyzed by flow cytometry. Finally,
to examine the effect of Aurora-A shRNA on proliferation and chemosensitivity against docetaxel in vivo , a s.c. tumor formation assay in nude mice was done.
Results: We established two genetically different stable cell lines (510 A and 1440 A) in which levels of Aurora-A were reduced. Cell
growth was inhibited by 38.7% in 510 A and by 24.3% in 1440 A in vitro compared with empty vector–transfected controls (510 m and 1440 m), and this growth inhibition was mediated through G 2 -M arrest as confirmed by flow cytometry. Next, in a WST assay, the IC 50 for Aurora-A shRNA-transfected cells was lower than that of empty vector–transfected cells (510 A, 2.7 × 10 −7 mol/L; 510 m, 4.8 × 10 −7 mol/L; 1440 A, 2.6 × 10 −7 mol/L; 1440 m, 4.9 × 10 −7 mol/L). In addition, 0.3 nmol/L docetaxel induced a notable level of apoptosis in Aurora-A shRNA-transfected cells compared
with empty vector–transfected cells. In the assay of s.c. tumors in nude mice, tumor growth in 510 A was inhibited by 36.1%
compared with that in 510 m, and in tumors treated with docetaxel, the suppression of Aurora-A resulted in 44.0% tumor growth
suppression in vivo .
Conclusions: These results indicated that Aurora-A might play an important role in chemosensitivity to docetaxel, and the suppression
of its expression might be a potential therapeutic target for ESCC.</description><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Aurora Kinase A</subject><subject>Aurora Kinases</subject><subject>Aurora-A</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Squamous Cell - drug therapy</subject><subject>Carcinoma, Squamous Cell - enzymology</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>chemosensitivity</subject><subject>Esophageal Neoplasms - drug therapy</subject><subject>Esophageal Neoplasms - enzymology</subject><subject>Esophageal Neoplasms - pathology</subject><subject>esophageal squamous cell carcinoma</subject><subject>Esophagus</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Nude</subject><subject>Pharmacology. Drug treatments</subject><subject>Protein-Serine-Threonine Kinases - antagonists & inhibitors</subject><subject>Protein-Serine-Threonine Kinases - biosynthesis</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>RNA, Small Interfering - genetics</subject><subject>shRNA</subject><subject>Taxoids - metabolism</subject><subject>Taxoids - pharmacology</subject><subject>Tumors</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkc1u1DAURi0EoqXwCCBvQGzS8V9iZzmEgaJWQmKGtWWbm8YoiVM7gXbPg-NoBrq5vovz2Z-OEXpNySWlpdpQIlVBBGeXTfOtIFVBac2eoHNalrLgrCqf5v0fc4ZepPSTECooEc_RGZWcSiXKc_Tn0AHeL9MUISUfRhxavF1iiKbYbvaHa1puPhy213h3_5_YjZ0ZHSTcdDCEBGPys__l5wc8B_wxOJjNPfTYj_hqGUzmU5g6cwumx_u7xQxhyVHoe9yY6PwYBvMSPWtNn-DV6bxA3z_tDs1VcfP185dme1M4ofhcSMvAsarmjLSCVLy1FlrLK6Fqw6yQjFuQhgulFFiumG0FEFspA1zVTAh-gd4d751iuFsgzXrwyeUqZoTcSlc1EUTULIPlEXQxpBSh1VP0g4kPmhK96terWr2q1Vm_JpVe9efcm9MDix3gx2Pq5DsDb0-ASc70bcwmfXrklCSEcJm590eu87fdbx9Bu9V5zH8A2VqnKdciD075X4SGnAc</recordid><startdate>20070215</startdate><enddate>20070215</enddate><creator>TANAKA, Eiji</creator><creator>HASHIMOTO, Yosuke</creator><creator>ITO, Tetsuo</creator><creator>KONDO, Kan</creator><creator>HIGASHIYAMA, Motoshige</creator><creator>TSUNODA, Shigeru</creator><creator>ORTIZ, Cristian</creator><creator>SAKAI, Yoshiharu</creator><creator>INAZAWA, Johji</creator><creator>SHIMADA, Yutaka</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><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>20070215</creationdate><title>The Suppression of Aurora-A/STK15/BTAK Expression Enhances Chemosensitivity to Docetaxel in Human Esophageal Squamous Cell Carcinoma</title><author>TANAKA, Eiji ; HASHIMOTO, Yosuke ; ITO, Tetsuo ; KONDO, Kan ; HIGASHIYAMA, Motoshige ; TSUNODA, Shigeru ; ORTIZ, Cristian ; SAKAI, Yoshiharu ; INAZAWA, Johji ; SHIMADA, Yutaka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c483t-7b2ec269320f4063fbbefb36489a2b4723be7a34888eb382bf4e0b68ae3892443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Aurora Kinase A</topic><topic>Aurora Kinases</topic><topic>Aurora-A</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Squamous Cell - drug therapy</topic><topic>Carcinoma, Squamous Cell - enzymology</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>chemosensitivity</topic><topic>Esophageal Neoplasms - drug therapy</topic><topic>Esophageal Neoplasms - enzymology</topic><topic>Esophageal Neoplasms - pathology</topic><topic>esophageal squamous cell carcinoma</topic><topic>Esophagus</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Nude</topic><topic>Pharmacology. Drug treatments</topic><topic>Protein-Serine-Threonine Kinases - antagonists & inhibitors</topic><topic>Protein-Serine-Threonine Kinases - biosynthesis</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Protein-Serine-Threonine Kinases - metabolism</topic><topic>RNA, Small Interfering - genetics</topic><topic>shRNA</topic><topic>Taxoids - metabolism</topic><topic>Taxoids - pharmacology</topic><topic>Tumors</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>TANAKA, Eiji</creatorcontrib><creatorcontrib>HASHIMOTO, Yosuke</creatorcontrib><creatorcontrib>ITO, Tetsuo</creatorcontrib><creatorcontrib>KONDO, Kan</creatorcontrib><creatorcontrib>HIGASHIYAMA, Motoshige</creatorcontrib><creatorcontrib>TSUNODA, Shigeru</creatorcontrib><creatorcontrib>ORTIZ, Cristian</creatorcontrib><creatorcontrib>SAKAI, Yoshiharu</creatorcontrib><creatorcontrib>INAZAWA, Johji</creatorcontrib><creatorcontrib>SHIMADA, Yutaka</creatorcontrib><collection>Pascal-Francis</collection><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>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>TANAKA, Eiji</au><au>HASHIMOTO, Yosuke</au><au>ITO, Tetsuo</au><au>KONDO, Kan</au><au>HIGASHIYAMA, Motoshige</au><au>TSUNODA, Shigeru</au><au>ORTIZ, Cristian</au><au>SAKAI, Yoshiharu</au><au>INAZAWA, Johji</au><au>SHIMADA, Yutaka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Suppression of Aurora-A/STK15/BTAK Expression Enhances Chemosensitivity to Docetaxel in Human Esophageal Squamous Cell Carcinoma</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2007-02-15</date><risdate>2007</risdate><volume>13</volume><issue>4</issue><spage>1331</spage><epage>1340</epage><pages>1331-1340</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Purpose: We previously reported that the expression of Aurora-A was frequently up-regulated in human esophageal squamous cell carcinoma
(ESCC) tissues as well as cell lines and the up-regulation contributed to a poor prognosis. In this study, we assessed the
possibility of Aurora-A suppression as a therapeutic target for ESCC using ESCC cell lines.
Experimental Design: We established subclones using vector-based short hairpin RNA (shRNA). Then, we investigated the effect of Aurora-A suppression
on proliferation and cell cycle changes in vitro . Next, chemosensitivity against docetaxel was investigated by tetrazolium salt–based proliferation assay (WST assay) and
cell number determinations, and furthermore, the type of cell death induced by docetaxel was analyzed by flow cytometry. Finally,
to examine the effect of Aurora-A shRNA on proliferation and chemosensitivity against docetaxel in vivo , a s.c. tumor formation assay in nude mice was done.
Results: We established two genetically different stable cell lines (510 A and 1440 A) in which levels of Aurora-A were reduced. Cell
growth was inhibited by 38.7% in 510 A and by 24.3% in 1440 A in vitro compared with empty vector–transfected controls (510 m and 1440 m), and this growth inhibition was mediated through G 2 -M arrest as confirmed by flow cytometry. Next, in a WST assay, the IC 50 for Aurora-A shRNA-transfected cells was lower than that of empty vector–transfected cells (510 A, 2.7 × 10 −7 mol/L; 510 m, 4.8 × 10 −7 mol/L; 1440 A, 2.6 × 10 −7 mol/L; 1440 m, 4.9 × 10 −7 mol/L). In addition, 0.3 nmol/L docetaxel induced a notable level of apoptosis in Aurora-A shRNA-transfected cells compared
with empty vector–transfected cells. In the assay of s.c. tumors in nude mice, tumor growth in 510 A was inhibited by 36.1%
compared with that in 510 m, and in tumors treated with docetaxel, the suppression of Aurora-A resulted in 44.0% tumor growth
suppression in vivo .
Conclusions: These results indicated that Aurora-A might play an important role in chemosensitivity to docetaxel, and the suppression
of its expression might be a potential therapeutic target for ESCC.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>17317845</pmid><doi>10.1158/1078-0432.CCR-06-1192</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Clinical cancer research, 2007-02, Vol.13 (4), p.1331-1340 |
| issn | 1078-0432 1557-3265 |
| language | eng |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Antineoplastic agents Antineoplastic Agents - pharmacology Aurora Kinase A Aurora Kinases Aurora-A Biological and medical sciences Carcinoma, Squamous Cell - drug therapy Carcinoma, Squamous Cell - enzymology Carcinoma, Squamous Cell - pathology Cell Line, Tumor chemosensitivity Esophageal Neoplasms - drug therapy Esophageal Neoplasms - enzymology Esophageal Neoplasms - pathology esophageal squamous cell carcinoma Esophagus Gastroenterology. Liver. Pancreas. Abdomen Humans Male Medical sciences Mice Mice, Inbred BALB C Mice, Nude Pharmacology. Drug treatments Protein-Serine-Threonine Kinases - antagonists & inhibitors Protein-Serine-Threonine Kinases - biosynthesis Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - metabolism RNA, Small Interfering - genetics shRNA Taxoids - metabolism Taxoids - pharmacology Tumors Xenograft Model Antitumor Assays |
| title | The Suppression of Aurora-A/STK15/BTAK Expression Enhances Chemosensitivity to Docetaxel in Human Esophageal Squamous Cell Carcinoma |
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