Study of molecular markers of resistance to m-AMSA in a human breast cancer cell line : Decrease of topoisomerase II and increase of both topoisomerase I and acidic glutathione S transferase
Resistance to 0.8 μM 4′′-(9-acridinylamino)methanesulphon- m-anisidide ( m-AMSA) was induced by stepwise increases of drug concentration in the human tumor cell line CALc18 originating from a breast adenocarcinoma. The resistant cell line CALc18/AMSA exhibited a resistance index of 10 and a cross-re...
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| Veröffentlicht in: | Biochemical pharmacology 1991-06, Vol.41 (12), p.1967-1979 |
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| container_end_page | 1979 |
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| container_title | Biochemical pharmacology |
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| creator | Lefevre, Dominique Riou, Jean-François Ahomadegbe, Jean Charles Zhou, Danyi Benard, Jean Riou, Guy |
| description | Resistance to 0.8 μM 4′′-(9-acridinylamino)methanesulphon-
m-anisidide (
m-AMSA) was induced by stepwise increases of drug concentration in the human tumor cell line CALc18 originating from a breast adenocarcinoma. The resistant cell line CALc18/AMSA exhibited a resistance index of 10 and a cross-resistance to other topoisomerase II inhibitors. A 3-fold decrease in the levels of topoisomerase II decatenating activity was found in CALc18/AMSA cells. By contrast, topoisomerase I activity was increased by about 3-fold in resistant cells. Interestingly this line was hypersensitive to camptothecin, a specific inhibitor of topoisomerase I. Restriction endonuclease patterns of the topoisomerase I and topoisomerase II loci were found to be identical in CALc18/AMSA and CALc18 with no evidence of gene amplification and rearrangements. Alkaline elution of
m-AMSA-treated cells showed that DNA single strand breaks and DNA-protein crosslinks were decreased in CALc18/AMSA. The DNA lesions also obtained in
m-AMSA-treated nuclei indicated that no drug uptake modification occurred in both cells. Moreover, the
in vitro
m-AMSA-induced DNA cleavage per unit of decatenating activity and the inhibitory effects of antitumoral drugs on decatenation were not found to be different with topoisomerase II from sensitive or resistant cells. However the specific cleavage induced by
m-AMSA/per mg of crude protein from resistant cells was 2 to 3 times decreased. Multidrug resistance gene transcripts were not detected while levels of acidic glutathione
S transferase mRNA were found to be 8 to 10-fold greater in resistant than in sensitive cell line with no amplification of the gene. In conclusion, the diminution of topoisomerase II activity and the increase of both topoisomerase I and acidic glutathione
S transferase transcripts could contribute to the resistant phenotype of these breast cancer cells. |
| doi_str_mv | 10.1016/0006-2952(91)90138-U |
| format | Article |
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m-anisidide (
m-AMSA) was induced by stepwise increases of drug concentration in the human tumor cell line CALc18 originating from a breast adenocarcinoma. The resistant cell line CALc18/AMSA exhibited a resistance index of 10 and a cross-resistance to other topoisomerase II inhibitors. A 3-fold decrease in the levels of topoisomerase II decatenating activity was found in CALc18/AMSA cells. By contrast, topoisomerase I activity was increased by about 3-fold in resistant cells. Interestingly this line was hypersensitive to camptothecin, a specific inhibitor of topoisomerase I. Restriction endonuclease patterns of the topoisomerase I and topoisomerase II loci were found to be identical in CALc18/AMSA and CALc18 with no evidence of gene amplification and rearrangements. Alkaline elution of
m-AMSA-treated cells showed that DNA single strand breaks and DNA-protein crosslinks were decreased in CALc18/AMSA. The DNA lesions also obtained in
m-AMSA-treated nuclei indicated that no drug uptake modification occurred in both cells. Moreover, the
in vitro
m-AMSA-induced DNA cleavage per unit of decatenating activity and the inhibitory effects of antitumoral drugs on decatenation were not found to be different with topoisomerase II from sensitive or resistant cells. However the specific cleavage induced by
m-AMSA/per mg of crude protein from resistant cells was 2 to 3 times decreased. Multidrug resistance gene transcripts were not detected while levels of acidic glutathione
S transferase mRNA were found to be 8 to 10-fold greater in resistant than in sensitive cell line with no amplification of the gene. In conclusion, the diminution of topoisomerase II activity and the increase of both topoisomerase I and acidic glutathione
S transferase transcripts could contribute to the resistant phenotype of these breast cancer cells.</description><identifier>ISSN: 0006-2952</identifier><identifier>EISSN: 1873-2968</identifier><identifier>DOI: 10.1016/0006-2952(91)90138-U</identifier><identifier>PMID: 1645555</identifier><identifier>CODEN: BCPCA6</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adenocarcinoma - enzymology ; Adenocarcinoma - genetics ; Adenocarcinoma - pathology ; Amsacrine - pharmacology ; Animals ; Antineoplastic agents ; Biological and medical sciences ; Biomarkers, Tumor ; Breast Neoplasms - drug therapy ; Breast Neoplasms - enzymology ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Chemotherapy ; DNA Damage ; DNA Topoisomerases, Type I - genetics ; DNA Topoisomerases, Type I - metabolism ; DNA Topoisomerases, Type II - genetics ; DNA Topoisomerases, Type II - metabolism ; DNA, Neoplasm - drug effects ; DNA, Neoplasm - metabolism ; Drug Resistance - genetics ; Female ; Gene Expression ; Glutathione Transferase - genetics ; Glutathione Transferase - metabolism ; Humans ; Medical sciences ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Pharmacology. Drug treatments ; Tumor Cells, Cultured</subject><ispartof>Biochemical pharmacology, 1991-06, Vol.41 (12), p.1967-1979</ispartof><rights>1991</rights><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/000629529190138U$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19730625$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1645555$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lefevre, Dominique</creatorcontrib><creatorcontrib>Riou, Jean-François</creatorcontrib><creatorcontrib>Ahomadegbe, Jean Charles</creatorcontrib><creatorcontrib>Zhou, Danyi</creatorcontrib><creatorcontrib>Benard, Jean</creatorcontrib><creatorcontrib>Riou, Guy</creatorcontrib><title>Study of molecular markers of resistance to m-AMSA in a human breast cancer cell line : Decrease of topoisomerase II and increase of both topoisomerase I and acidic glutathione S transferase</title><title>Biochemical pharmacology</title><addtitle>Biochem Pharmacol</addtitle><description>Resistance to 0.8 μM 4′′-(9-acridinylamino)methanesulphon-
m-anisidide (
m-AMSA) was induced by stepwise increases of drug concentration in the human tumor cell line CALc18 originating from a breast adenocarcinoma. The resistant cell line CALc18/AMSA exhibited a resistance index of 10 and a cross-resistance to other topoisomerase II inhibitors. A 3-fold decrease in the levels of topoisomerase II decatenating activity was found in CALc18/AMSA cells. By contrast, topoisomerase I activity was increased by about 3-fold in resistant cells. Interestingly this line was hypersensitive to camptothecin, a specific inhibitor of topoisomerase I. Restriction endonuclease patterns of the topoisomerase I and topoisomerase II loci were found to be identical in CALc18/AMSA and CALc18 with no evidence of gene amplification and rearrangements. Alkaline elution of
m-AMSA-treated cells showed that DNA single strand breaks and DNA-protein crosslinks were decreased in CALc18/AMSA. The DNA lesions also obtained in
m-AMSA-treated nuclei indicated that no drug uptake modification occurred in both cells. Moreover, the
in vitro
m-AMSA-induced DNA cleavage per unit of decatenating activity and the inhibitory effects of antitumoral drugs on decatenation were not found to be different with topoisomerase II from sensitive or resistant cells. However the specific cleavage induced by
m-AMSA/per mg of crude protein from resistant cells was 2 to 3 times decreased. Multidrug resistance gene transcripts were not detected while levels of acidic glutathione
S transferase mRNA were found to be 8 to 10-fold greater in resistant than in sensitive cell line with no amplification of the gene. In conclusion, the diminution of topoisomerase II activity and the increase of both topoisomerase I and acidic glutathione
S transferase transcripts could contribute to the resistant phenotype of these breast cancer cells.</description><subject>Adenocarcinoma - enzymology</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - pathology</subject><subject>Amsacrine - pharmacology</subject><subject>Animals</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - enzymology</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Chemotherapy</subject><subject>DNA Damage</subject><subject>DNA Topoisomerases, Type I - genetics</subject><subject>DNA Topoisomerases, Type I - metabolism</subject><subject>DNA Topoisomerases, Type II - genetics</subject><subject>DNA Topoisomerases, Type II - metabolism</subject><subject>DNA, Neoplasm - drug effects</subject><subject>DNA, Neoplasm - metabolism</subject><subject>Drug Resistance - genetics</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Glutathione Transferase - genetics</subject><subject>Glutathione Transferase - metabolism</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Neoplasm Transplantation</subject><subject>Pharmacology. Drug treatments</subject><subject>Tumor Cells, Cultured</subject><issn>0006-2952</issn><issn>1873-2968</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkt2KFDEQhYMo67j6Bgq5UfSitdI_6cQLYVj_Bla8GOc6ZNIVJ9rdGZO0sC_ns5nMDi6YmyJ1Pg6cqiLkKYPXDBh_AwC8qmVXv5TslQTWiGp3j6yY6Jvc5uI-Wf1DHpJHMf4oX8HZBblgvO3yW5E_27QMN9RbOvkRzTLqQCcdfmKIpRkwupj0bJAmT6dq_WW7pm6mmh6WSc90H1DHRE0hAjU4jnR0M9K39D2aomFxSf7oXfQThtLYbKieh-xyB-x9OvxPnSBt3OAM_T4uSaeD89l6S1PQc7Qn7DF5YPUY8cm5XpLdxw_frj5X118_ba7W1xXWwFOFvTF7QNML5KxDYwfsGRrAxrCh5lJwwRjnYMFYIRBaQNsCt03HpdSDbS7Ji1vfY_C_FoxJTS6WuHpGv0QloBNtKyGDz87gsp9wUMfg8jhv1HngWX9-1nU0erQ5inHxDpN9A7wu3LtbDnOq3w6DisZhnvLgApqkBu8UA1UOQZW1qrJlJZk6HYLaNX8BPbinFg</recordid><startdate>19910615</startdate><enddate>19910615</enddate><creator>Lefevre, Dominique</creator><creator>Riou, Jean-François</creator><creator>Ahomadegbe, Jean Charles</creator><creator>Zhou, Danyi</creator><creator>Benard, Jean</creator><creator>Riou, Guy</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>19910615</creationdate><title>Study of molecular markers of resistance to m-AMSA in a human breast cancer cell line : Decrease of topoisomerase II and increase of both topoisomerase I and acidic glutathione S transferase</title><author>Lefevre, Dominique ; Riou, Jean-François ; Ahomadegbe, Jean Charles ; Zhou, Danyi ; Benard, Jean ; Riou, Guy</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e206t-e7ccb0ec78e615ecfde71ec0e3c1d26986811660f0cf88e040ef406f35699adf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Adenocarcinoma - enzymology</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - pathology</topic><topic>Amsacrine - pharmacology</topic><topic>Animals</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - enzymology</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>Chemotherapy</topic><topic>DNA Damage</topic><topic>DNA Topoisomerases, Type I - genetics</topic><topic>DNA Topoisomerases, Type I - metabolism</topic><topic>DNA Topoisomerases, Type II - genetics</topic><topic>DNA Topoisomerases, Type II - metabolism</topic><topic>DNA, Neoplasm - drug effects</topic><topic>DNA, Neoplasm - metabolism</topic><topic>Drug Resistance - genetics</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Glutathione Transferase - genetics</topic><topic>Glutathione Transferase - metabolism</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Neoplasm Transplantation</topic><topic>Pharmacology. Drug treatments</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lefevre, Dominique</creatorcontrib><creatorcontrib>Riou, Jean-François</creatorcontrib><creatorcontrib>Ahomadegbe, Jean Charles</creatorcontrib><creatorcontrib>Zhou, Danyi</creatorcontrib><creatorcontrib>Benard, Jean</creatorcontrib><creatorcontrib>Riou, Guy</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>MEDLINE - Academic</collection><jtitle>Biochemical pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lefevre, Dominique</au><au>Riou, Jean-François</au><au>Ahomadegbe, Jean Charles</au><au>Zhou, Danyi</au><au>Benard, Jean</au><au>Riou, Guy</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Study of molecular markers of resistance to m-AMSA in a human breast cancer cell line : Decrease of topoisomerase II and increase of both topoisomerase I and acidic glutathione S transferase</atitle><jtitle>Biochemical pharmacology</jtitle><addtitle>Biochem Pharmacol</addtitle><date>1991-06-15</date><risdate>1991</risdate><volume>41</volume><issue>12</issue><spage>1967</spage><epage>1979</epage><pages>1967-1979</pages><issn>0006-2952</issn><eissn>1873-2968</eissn><coden>BCPCA6</coden><abstract>Resistance to 0.8 μM 4′′-(9-acridinylamino)methanesulphon-
m-anisidide (
m-AMSA) was induced by stepwise increases of drug concentration in the human tumor cell line CALc18 originating from a breast adenocarcinoma. The resistant cell line CALc18/AMSA exhibited a resistance index of 10 and a cross-resistance to other topoisomerase II inhibitors. A 3-fold decrease in the levels of topoisomerase II decatenating activity was found in CALc18/AMSA cells. By contrast, topoisomerase I activity was increased by about 3-fold in resistant cells. Interestingly this line was hypersensitive to camptothecin, a specific inhibitor of topoisomerase I. Restriction endonuclease patterns of the topoisomerase I and topoisomerase II loci were found to be identical in CALc18/AMSA and CALc18 with no evidence of gene amplification and rearrangements. Alkaline elution of
m-AMSA-treated cells showed that DNA single strand breaks and DNA-protein crosslinks were decreased in CALc18/AMSA. The DNA lesions also obtained in
m-AMSA-treated nuclei indicated that no drug uptake modification occurred in both cells. Moreover, the
in vitro
m-AMSA-induced DNA cleavage per unit of decatenating activity and the inhibitory effects of antitumoral drugs on decatenation were not found to be different with topoisomerase II from sensitive or resistant cells. However the specific cleavage induced by
m-AMSA/per mg of crude protein from resistant cells was 2 to 3 times decreased. Multidrug resistance gene transcripts were not detected while levels of acidic glutathione
S transferase mRNA were found to be 8 to 10-fold greater in resistant than in sensitive cell line with no amplification of the gene. In conclusion, the diminution of topoisomerase II activity and the increase of both topoisomerase I and acidic glutathione
S transferase transcripts could contribute to the resistant phenotype of these breast cancer cells.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>1645555</pmid><doi>10.1016/0006-2952(91)90138-U</doi><tpages>13</tpages></addata></record> |
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| subjects | Adenocarcinoma - enzymology Adenocarcinoma - genetics Adenocarcinoma - pathology Amsacrine - pharmacology Animals Antineoplastic agents Biological and medical sciences Biomarkers, Tumor Breast Neoplasms - drug therapy Breast Neoplasms - enzymology Breast Neoplasms - genetics Breast Neoplasms - pathology Chemotherapy DNA Damage DNA Topoisomerases, Type I - genetics DNA Topoisomerases, Type I - metabolism DNA Topoisomerases, Type II - genetics DNA Topoisomerases, Type II - metabolism DNA, Neoplasm - drug effects DNA, Neoplasm - metabolism Drug Resistance - genetics Female Gene Expression Glutathione Transferase - genetics Glutathione Transferase - metabolism Humans Medical sciences Mice Mice, Nude Neoplasm Transplantation Pharmacology. Drug treatments Tumor Cells, Cultured |
| title | Study of molecular markers of resistance to m-AMSA in a human breast cancer cell line : Decrease of topoisomerase II and increase of both topoisomerase I and acidic glutathione S transferase |
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