Non-coding rRNA-mediated preferential killing in cancer cells is enhanced by suppression of autophagy in non-transformed counterpart.
Identifieur interne : 000368 ( PubMed/Curation ); précédent : 000367; suivant : 000369Non-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
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<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>
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