Non-coding rRNA-mediated preferential killing in cancer cells is enhanced by suppression of autophagy in non-transformed counterpart.
Identifieur interne : 001468 ( Main/Exploration ); précédent : 001467; suivant : 001469Non-coding rRNA-mediated preferential killing in cancer cells is enhanced by suppression of autophagy in non-transformed counterpart.
Auteurs : C J Hwang [États-Unis] ; J R Fields ; Y-H ShiaoSource :
- Cell death & disease [ 2041-4889 ] ; 2011.
Descripteurs français
- KwdFr :
- MESH :
- métabolisme : ARN non traduit, ARN ribosomique, Oligonucléotides.
- pharmacologie : Chloroquine.
- toxicité : Oligonucléotides antisens.
- Animaux, Apoptose, Autophagie, Humains, Lignée cellulaire tumorale, Souris.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Oligonucleotides, RNA, Ribosomal, RNA, Untranslated.
- chemical , pharmacology : Chloroquine.
- chemical , toxicity : Oligonucleotides, Antisense.
- Animals, Apoptosis, Autophagy, Cell Line, Tumor, Humans, Mice.
Abstract
Interest to anticancer agents targeting rRNA biogenesis is growing. Cis-non-coding rRNAs, alternative to primary rRNA, have been shown to regulate rRNA biogenesis. We have recently detected bidirectional non-coding rRNAs that carry ribozyme-like properties. Anti-antisense oligonucleotides complementary to antisense non-coding rRNAs markedly stabilized the bidirectional transcripts and induced cell death in mouse lung cells. Here, we demonstrated that the same oligonucleotide killed mouse lung-cancer cells preferentially, compared with non-cancer sister lines, suggesting its potential utility for cancer treatment. A human version of anti-antisense oligonucleotide, complementary to an rDNA intergenic site, mediated apoptosis primarily in cancer cells. Autophagic activation was largely undifferentiable between the anti-antisense and other oligonucleotides and accounted for the undesired cytotoxicity in non-cancer cells. Co-treatment with chloroquine, an autophagy inhibitor, reduced cytotoxicity in the non-cancer cells, but retained the anti-antisense-mediated killings in cancer cells. Furthermore, the anti-antisense oligonucleotide stabilized bidirectional non-coding rRNAs predominantly in human cancer cells and perturbed rRNA biogenesis. Contributions of non-coding rRNAs to cell death were proven by transfection of in -vitro-synthesized transcripts. Taken together, cancer/non-cancer cells respond differently to stabilization of non-coding rRNAs, and such differential responses provide a window of opportunity to enhance anticancer efficacy.
DOI: 10.1038/cddis.2011.110
PubMed: 22158478
Affiliations:
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Le document en format XML
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Shiao</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2011">2011</date><idno type="RBID">pubmed:22158478</idno><idno type="pmid">22158478</idno><idno type="doi">10.1038/cddis.2011.110</idno><idno type="wicri:Area/PubMed/Corpus">000368</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000368</idno><idno type="wicri:Area/PubMed/Curation">000368</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000368</idno><idno type="wicri:Area/PubMed/Checkpoint">000364</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000364</idno><idno type="wicri:Area/Ncbi/Merge">000166</idno><idno type="wicri:Area/Ncbi/Curation">000166</idno><idno type="wicri:Area/Ncbi/Checkpoint">000166</idno><idno type="wicri:Area/Main/Merge">001470</idno><idno type="wicri:Area/Main/Curation">001468</idno><idno 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first="Y-H" last="Shiao">Y-H Shiao</name></author></analytic><series><title level="j">Cell death & disease</title><idno type="eISSN">2041-4889</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Autophagy</term><term>Cell Line, Tumor</term><term>Chloroquine (pharmacology)</term><term>Humans</term><term>Mice</term><term>Oligonucleotides (metabolism)</term><term>Oligonucleotides, Antisense (toxicity)</term><term>RNA, Ribosomal (metabolism)</term><term>RNA, Untranslated (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN non traduit (métabolisme)</term><term>ARN ribosomique (métabolisme)</term><term>Animaux</term><term>Apoptose</term><term>Autophagie</term><term>Chloroquine (pharmacologie)</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Oligonucléotides (métabolisme)</term><term>Oligonucléotides antisens (toxicité)</term><term>Souris</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Oligonucleotides</term><term>RNA, Ribosomal</term><term>RNA, Untranslated</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chloroquine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Oligonucleotides, Antisense</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN non traduit</term><term>ARN ribosomique</term><term>Oligonucléotides</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Oligonucléotides antisens</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Autophagy</term><term>Cell Line, Tumor</term><term>Humans</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire tumorale</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Interest to anticancer agents targeting rRNA biogenesis is growing. Cis-non-coding rRNAs, alternative to primary rRNA, have been shown to regulate rRNA biogenesis. We have recently detected bidirectional non-coding rRNAs that carry ribozyme-like properties. Anti-antisense oligonucleotides complementary to antisense non-coding rRNAs markedly stabilized the bidirectional transcripts and induced cell death in mouse lung cells. Here, we demonstrated that the same oligonucleotide killed mouse lung-cancer cells preferentially, compared with non-cancer sister lines, suggesting its potential utility for cancer treatment. A human version of anti-antisense oligonucleotide, complementary to an rDNA intergenic site, mediated apoptosis primarily in cancer cells. Autophagic activation was largely undifferentiable between the anti-antisense and other oligonucleotides and accounted for the undesired cytotoxicity in non-cancer cells. Co-treatment with chloroquine, an autophagy inhibitor, reduced cytotoxicity in the non-cancer cells, but retained the anti-antisense-mediated killings in cancer cells. Furthermore, the anti-antisense oligonucleotide stabilized bidirectional non-coding rRNAs predominantly in human cancer cells and perturbed rRNA biogenesis. Contributions of non-coding rRNAs to cell death were proven by transfection of in -vitro-synthesized transcripts. Taken together, cancer/non-cancer cells respond differently to stabilization of non-coding rRNAs, and such differential responses provide a window of opportunity to enhance anticancer efficacy.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><noCountry><name sortKey="Fields, J R" sort="Fields, J R" uniqKey="Fields J" first="J R" last="Fields">J R Fields</name><name sortKey="Shiao, Y H" sort="Shiao, Y H" uniqKey="Shiao Y" first="Y-H" last="Shiao">Y-H Shiao</name></noCountry><country name="États-Unis"><region name="Maryland"><name sortKey="Hwang, C J" sort="Hwang, C J" uniqKey="Hwang C" first="C J" last="Hwang">C J Hwang</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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