Overexpression of Bax Enhances Antitumor Activity of Chemotherapeutic Agents in Human Head and Neck Squamous Cell Carcinoma
Overexpression of the Bax protein in human head and neck squamous cell carcinoma A253 cells was reported to result in an increased sensitivity to various chemotherapeutic agents in vitro (Guo et al., Oncol. Res., 11: 91–99, 1999). In the present study, the relationship between Bax expression and res...
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| creator | Guo, B Cao, S Tóth, K Azrak, R G Rustum, Y M |
| description | Overexpression
of the Bax protein in human head and neck squamous cell carcinoma A253
cells was reported to result in an increased sensitivity to various
chemotherapeutic agents in vitro (Guo et al.,
Oncol. Res., 11: 91–99, 1999). In the present study,
the relationship between Bax expression and response to chemotherapy
was further investigated in vitro and in
vivo model systems. For in vitro study, A253,
A253/Vec (pcDNA3 vector transfectant), and A253/Bax (pcDNA3/Bax
transfectant, expressing 50-fold higher Bax protein than A253 and
A253/Vec) cells were exposed to various concentrations of raltitrexed
(a specific thymidylate synthase inhibitor) and SN-38 (a topoisomerase
I inhibitor) for 2 h, and cell growth inhibition was assessed by
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide clonogenic
assay. Compared to A253/Vec, A253/Bax cells exhibited 9.5- and
13.8-fold increases in sensitivity to raltitrexed and SN-38,
respectively. For in vivo study, A253/Vec and A253/Bax
tumor xenografts were established by s.c. injection of tumor cells into
nude mice. The antitumor activity and toxicity of raltitrexed (i.v.
push daily for 5 days) and irinotecan (a prodrug of SN-38; i.v.
push daily for 3 days) were evaluated. The maximum tolerated
doses of raltitrexed and irinotecan were 30 and 100 mg/kg/day,
respectively. At the maximum tolerated doses, minimal antitumor
activity was observed with raltitrexed, although irinotecan was more
active than raltitrexed against A253 or A253/Vec tumors. In contrast,
both raltitrexed and irinotecan were significantly more active against
A253/Bax xenografts than against A253/Vec xenografts; the yield for
complete tumor regression (cure) was 40% and 100% with raltitrexed
and irinotecan, respectively, with no significant toxicity.
Furthermore, the observed increase of antitumor activity in A253/Bax
tumors was associated with an enhanced induction of apoptosis in
vivo . The in vivo results demonstrated a proof
of the principal concept that selecting up-regulation of the
proapoptosis gene Bax can provide the basis for a greater therapeutic
efficacy to a variety of chemotherapeutic agents with different
structures and mechanisms of action. |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_pasca</sourceid><recordid>TN_cdi_pubmed_primary_10690558</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>10690558</sourcerecordid><originalsourceid>FETCH-LOGICAL-h267t-36d8bcc042b09af0767bffa1b9f9a39d094e4525bc3e0a50068a6d3b2f33f7be3</originalsourceid><addsrcrecordid>eNpF0D1PwzAQBuAIgWgp_AXkAbFFcuLYScYQFYpU0QGYo7Nzbgz5KHZSWvHnSdUilrsbHp30vmfeNOA89lko-Pl40zjxacTCiXfl3AelQRTQ6NKbBFSklPNk6v2stmhxt7HonOla0mnyADsybytoFTqStb3ph6azJFO92Zp-fyB5hU3XV2hhg0NvFMnW2PaOmJYshgbGiVASaEvyguqTvH4N0HSDIznWNcnBKtN2DVx7FxpqhzenPfPeH-dv-cJfrp6e82zpV6GIe5-JMpFK0SiUNAVNYxFLrSGQqU6BpSVNI4x4yKViSIFTKhIQJZOhZkzHEtnMuz3-3QyywbLYWNOA3Rd_LYzg7gTAKai1HbMb9-8YjaNIjOz-yCqzrr6NxUIdSrJjdzhmqgpRhEUcJOwXjnt17w</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Overexpression of Bax Enhances Antitumor Activity of Chemotherapeutic Agents in Human Head and Neck Squamous Cell Carcinoma</title><source>MEDLINE</source><source>American Association for Cancer Research</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Guo, B ; Cao, S ; Tóth, K ; Azrak, R G ; Rustum, Y M</creator><creatorcontrib>Guo, B ; Cao, S ; Tóth, K ; Azrak, R G ; Rustum, Y M</creatorcontrib><description>Overexpression
of the Bax protein in human head and neck squamous cell carcinoma A253
cells was reported to result in an increased sensitivity to various
chemotherapeutic agents in vitro (Guo et al.,
Oncol. Res., 11: 91–99, 1999). In the present study,
the relationship between Bax expression and response to chemotherapy
was further investigated in vitro and in
vivo model systems. For in vitro study, A253,
A253/Vec (pcDNA3 vector transfectant), and A253/Bax (pcDNA3/Bax
transfectant, expressing 50-fold higher Bax protein than A253 and
A253/Vec) cells were exposed to various concentrations of raltitrexed
(a specific thymidylate synthase inhibitor) and SN-38 (a topoisomerase
I inhibitor) for 2 h, and cell growth inhibition was assessed by
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide clonogenic
assay. Compared to A253/Vec, A253/Bax cells exhibited 9.5- and
13.8-fold increases in sensitivity to raltitrexed and SN-38,
respectively. For in vivo study, A253/Vec and A253/Bax
tumor xenografts were established by s.c. injection of tumor cells into
nude mice. The antitumor activity and toxicity of raltitrexed (i.v.
push daily for 5 days) and irinotecan (a prodrug of SN-38; i.v.
push daily for 3 days) were evaluated. The maximum tolerated
doses of raltitrexed and irinotecan were 30 and 100 mg/kg/day,
respectively. At the maximum tolerated doses, minimal antitumor
activity was observed with raltitrexed, although irinotecan was more
active than raltitrexed against A253 or A253/Vec tumors. In contrast,
both raltitrexed and irinotecan were significantly more active against
A253/Bax xenografts than against A253/Vec xenografts; the yield for
complete tumor regression (cure) was 40% and 100% with raltitrexed
and irinotecan, respectively, with no significant toxicity.
Furthermore, the observed increase of antitumor activity in A253/Bax
tumors was associated with an enhanced induction of apoptosis in
vivo . The in vivo results demonstrated a proof
of the principal concept that selecting up-regulation of the
proapoptosis gene Bax can provide the basis for a greater therapeutic
efficacy to a variety of chemotherapeutic agents with different
structures and mechanisms of action.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>PMID: 10690558</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Animals ; Antimetabolites, Antineoplastic - therapeutic use ; Antimetabolites, Antineoplastic - toxicity ; Antineoplastic agents ; Antineoplastic Agents, Phytogenic - therapeutic use ; Antineoplastic Agents, Phytogenic - toxicity ; Apoptosis - drug effects ; bcl-2-Associated X Protein ; Biological and medical sciences ; Camptothecin - analogs & derivatives ; Camptothecin - therapeutic use ; Camptothecin - toxicity ; Carcinoma, Squamous Cell - drug therapy ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - pathology ; Cell Division - drug effects ; Cell Survival - drug effects ; Chemotherapy ; Enzyme Inhibitors - therapeutic use ; Female ; Head and Neck Neoplasms - drug therapy ; Head and Neck Neoplasms - genetics ; Head and Neck Neoplasms - pathology ; Humans ; Medical sciences ; Mice ; Mice, Nude ; Pharmacology. Drug treatments ; Proto-Oncogene Proteins - biosynthesis ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins c-bcl-2 ; Quinazolines - therapeutic use ; Quinazolines - toxicity ; Thiophenes - therapeutic use ; Thiophenes - toxicity ; Thymidylate Synthase - antagonists & inhibitors ; Topoisomerase I Inhibitors ; Transplantation, Heterologous ; Tumor Cells, Cultured</subject><ispartof>Clinical cancer research, 2000-02, Vol.6 (2), p.718-724</ispartof><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1307446$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10690558$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, B</creatorcontrib><creatorcontrib>Cao, S</creatorcontrib><creatorcontrib>Tóth, K</creatorcontrib><creatorcontrib>Azrak, R G</creatorcontrib><creatorcontrib>Rustum, Y M</creatorcontrib><title>Overexpression of Bax Enhances Antitumor Activity of Chemotherapeutic Agents in Human Head and Neck Squamous Cell Carcinoma</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Overexpression
of the Bax protein in human head and neck squamous cell carcinoma A253
cells was reported to result in an increased sensitivity to various
chemotherapeutic agents in vitro (Guo et al.,
Oncol. Res., 11: 91–99, 1999). In the present study,
the relationship between Bax expression and response to chemotherapy
was further investigated in vitro and in
vivo model systems. For in vitro study, A253,
A253/Vec (pcDNA3 vector transfectant), and A253/Bax (pcDNA3/Bax
transfectant, expressing 50-fold higher Bax protein than A253 and
A253/Vec) cells were exposed to various concentrations of raltitrexed
(a specific thymidylate synthase inhibitor) and SN-38 (a topoisomerase
I inhibitor) for 2 h, and cell growth inhibition was assessed by
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide clonogenic
assay. Compared to A253/Vec, A253/Bax cells exhibited 9.5- and
13.8-fold increases in sensitivity to raltitrexed and SN-38,
respectively. For in vivo study, A253/Vec and A253/Bax
tumor xenografts were established by s.c. injection of tumor cells into
nude mice. The antitumor activity and toxicity of raltitrexed (i.v.
push daily for 5 days) and irinotecan (a prodrug of SN-38; i.v.
push daily for 3 days) were evaluated. The maximum tolerated
doses of raltitrexed and irinotecan were 30 and 100 mg/kg/day,
respectively. At the maximum tolerated doses, minimal antitumor
activity was observed with raltitrexed, although irinotecan was more
active than raltitrexed against A253 or A253/Vec tumors. In contrast,
both raltitrexed and irinotecan were significantly more active against
A253/Bax xenografts than against A253/Vec xenografts; the yield for
complete tumor regression (cure) was 40% and 100% with raltitrexed
and irinotecan, respectively, with no significant toxicity.
Furthermore, the observed increase of antitumor activity in A253/Bax
tumors was associated with an enhanced induction of apoptosis in
vivo . The in vivo results demonstrated a proof
of the principal concept that selecting up-regulation of the
proapoptosis gene Bax can provide the basis for a greater therapeutic
efficacy to a variety of chemotherapeutic agents with different
structures and mechanisms of action.</description><subject>Animals</subject><subject>Antimetabolites, Antineoplastic - therapeutic use</subject><subject>Antimetabolites, Antineoplastic - toxicity</subject><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents, Phytogenic - therapeutic use</subject><subject>Antineoplastic Agents, Phytogenic - toxicity</subject><subject>Apoptosis - drug effects</subject><subject>bcl-2-Associated X Protein</subject><subject>Biological and medical sciences</subject><subject>Camptothecin - analogs & derivatives</subject><subject>Camptothecin - therapeutic use</subject><subject>Camptothecin - toxicity</subject><subject>Carcinoma, Squamous Cell - drug therapy</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell Division - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Chemotherapy</subject><subject>Enzyme Inhibitors - therapeutic use</subject><subject>Female</subject><subject>Head and Neck Neoplasms - drug therapy</subject><subject>Head and Neck Neoplasms - genetics</subject><subject>Head and Neck Neoplasms - pathology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Pharmacology. Drug treatments</subject><subject>Proto-Oncogene Proteins - biosynthesis</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2</subject><subject>Quinazolines - therapeutic use</subject><subject>Quinazolines - toxicity</subject><subject>Thiophenes - therapeutic use</subject><subject>Thiophenes - toxicity</subject><subject>Thymidylate Synthase - antagonists & inhibitors</subject><subject>Topoisomerase I Inhibitors</subject><subject>Transplantation, Heterologous</subject><subject>Tumor Cells, Cultured</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0D1PwzAQBuAIgWgp_AXkAbFFcuLYScYQFYpU0QGYo7Nzbgz5KHZSWvHnSdUilrsbHp30vmfeNOA89lko-Pl40zjxacTCiXfl3AelQRTQ6NKbBFSklPNk6v2stmhxt7HonOla0mnyADsybytoFTqStb3ph6azJFO92Zp-fyB5hU3XV2hhg0NvFMnW2PaOmJYshgbGiVASaEvyguqTvH4N0HSDIznWNcnBKtN2DVx7FxpqhzenPfPeH-dv-cJfrp6e82zpV6GIe5-JMpFK0SiUNAVNYxFLrSGQqU6BpSVNI4x4yKViSIFTKhIQJZOhZkzHEtnMuz3-3QyywbLYWNOA3Rd_LYzg7gTAKai1HbMb9-8YjaNIjOz-yCqzrr6NxUIdSrJjdzhmqgpRhEUcJOwXjnt17w</recordid><startdate>20000201</startdate><enddate>20000201</enddate><creator>Guo, B</creator><creator>Cao, S</creator><creator>Tóth, K</creator><creator>Azrak, R G</creator><creator>Rustum, Y M</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></search><sort><creationdate>20000201</creationdate><title>Overexpression of Bax Enhances Antitumor Activity of Chemotherapeutic Agents in Human Head and Neck Squamous Cell Carcinoma</title><author>Guo, B ; Cao, S ; Tóth, K ; Azrak, R G ; Rustum, Y M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h267t-36d8bcc042b09af0767bffa1b9f9a39d094e4525bc3e0a50068a6d3b2f33f7be3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Antimetabolites, Antineoplastic - therapeutic use</topic><topic>Antimetabolites, Antineoplastic - toxicity</topic><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents, Phytogenic - therapeutic use</topic><topic>Antineoplastic Agents, Phytogenic - toxicity</topic><topic>Apoptosis - drug effects</topic><topic>bcl-2-Associated X Protein</topic><topic>Biological and medical sciences</topic><topic>Camptothecin - analogs & derivatives</topic><topic>Camptothecin - therapeutic use</topic><topic>Camptothecin - toxicity</topic><topic>Carcinoma, Squamous Cell - drug therapy</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell Division - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Chemotherapy</topic><topic>Enzyme Inhibitors - therapeutic use</topic><topic>Female</topic><topic>Head and Neck Neoplasms - drug therapy</topic><topic>Head and Neck Neoplasms - genetics</topic><topic>Head and Neck Neoplasms - pathology</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Pharmacology. Drug treatments</topic><topic>Proto-Oncogene Proteins - biosynthesis</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins c-bcl-2</topic><topic>Quinazolines - therapeutic use</topic><topic>Quinazolines - toxicity</topic><topic>Thiophenes - therapeutic use</topic><topic>Thiophenes - toxicity</topic><topic>Thymidylate Synthase - antagonists & inhibitors</topic><topic>Topoisomerase I Inhibitors</topic><topic>Transplantation, Heterologous</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, B</creatorcontrib><creatorcontrib>Cao, S</creatorcontrib><creatorcontrib>Tóth, K</creatorcontrib><creatorcontrib>Azrak, R G</creatorcontrib><creatorcontrib>Rustum, Y M</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, B</au><au>Cao, S</au><au>Tóth, K</au><au>Azrak, R G</au><au>Rustum, Y M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of Bax Enhances Antitumor Activity of Chemotherapeutic Agents in Human Head and Neck Squamous Cell Carcinoma</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2000-02-01</date><risdate>2000</risdate><volume>6</volume><issue>2</issue><spage>718</spage><epage>724</epage><pages>718-724</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Overexpression
of the Bax protein in human head and neck squamous cell carcinoma A253
cells was reported to result in an increased sensitivity to various
chemotherapeutic agents in vitro (Guo et al.,
Oncol. Res., 11: 91–99, 1999). In the present study,
the relationship between Bax expression and response to chemotherapy
was further investigated in vitro and in
vivo model systems. For in vitro study, A253,
A253/Vec (pcDNA3 vector transfectant), and A253/Bax (pcDNA3/Bax
transfectant, expressing 50-fold higher Bax protein than A253 and
A253/Vec) cells were exposed to various concentrations of raltitrexed
(a specific thymidylate synthase inhibitor) and SN-38 (a topoisomerase
I inhibitor) for 2 h, and cell growth inhibition was assessed by
3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide clonogenic
assay. Compared to A253/Vec, A253/Bax cells exhibited 9.5- and
13.8-fold increases in sensitivity to raltitrexed and SN-38,
respectively. For in vivo study, A253/Vec and A253/Bax
tumor xenografts were established by s.c. injection of tumor cells into
nude mice. The antitumor activity and toxicity of raltitrexed (i.v.
push daily for 5 days) and irinotecan (a prodrug of SN-38; i.v.
push daily for 3 days) were evaluated. The maximum tolerated
doses of raltitrexed and irinotecan were 30 and 100 mg/kg/day,
respectively. At the maximum tolerated doses, minimal antitumor
activity was observed with raltitrexed, although irinotecan was more
active than raltitrexed against A253 or A253/Vec tumors. In contrast,
both raltitrexed and irinotecan were significantly more active against
A253/Bax xenografts than against A253/Vec xenografts; the yield for
complete tumor regression (cure) was 40% and 100% with raltitrexed
and irinotecan, respectively, with no significant toxicity.
Furthermore, the observed increase of antitumor activity in A253/Bax
tumors was associated with an enhanced induction of apoptosis in
vivo . The in vivo results demonstrated a proof
of the principal concept that selecting up-regulation of the
proapoptosis gene Bax can provide the basis for a greater therapeutic
efficacy to a variety of chemotherapeutic agents with different
structures and mechanisms of action.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>10690558</pmid><tpages>7</tpages></addata></record> |
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| identifier | ISSN: 1078-0432 |
| ispartof | Clinical cancer research, 2000-02, Vol.6 (2), p.718-724 |
| issn | 1078-0432 1557-3265 |
| language | eng |
| recordid | cdi_pubmed_primary_10690558 |
| source | MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Antimetabolites, Antineoplastic - therapeutic use Antimetabolites, Antineoplastic - toxicity Antineoplastic agents Antineoplastic Agents, Phytogenic - therapeutic use Antineoplastic Agents, Phytogenic - toxicity Apoptosis - drug effects bcl-2-Associated X Protein Biological and medical sciences Camptothecin - analogs & derivatives Camptothecin - therapeutic use Camptothecin - toxicity Carcinoma, Squamous Cell - drug therapy Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - pathology Cell Division - drug effects Cell Survival - drug effects Chemotherapy Enzyme Inhibitors - therapeutic use Female Head and Neck Neoplasms - drug therapy Head and Neck Neoplasms - genetics Head and Neck Neoplasms - pathology Humans Medical sciences Mice Mice, Nude Pharmacology. Drug treatments Proto-Oncogene Proteins - biosynthesis Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins c-bcl-2 Quinazolines - therapeutic use Quinazolines - toxicity Thiophenes - therapeutic use Thiophenes - toxicity Thymidylate Synthase - antagonists & inhibitors Topoisomerase I Inhibitors Transplantation, Heterologous Tumor Cells, Cultured |
| title | Overexpression of Bax Enhances Antitumor Activity of Chemotherapeutic Agents in Human Head and Neck Squamous Cell Carcinoma |
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