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A novel long non-coding RNA T-ALL-R-LncR1 knockdown and Par-4 cooperate to induce cellular apoptosis in T-cell acute lymphoblastic leukemia cells.
- Source :
-
Leukemia & Lymphoma . Jun2014, Vol. 55 Issue 6, p1373-1382. 10p. - Publication Year :
- 2014
-
Abstract
- T-cell acute lymphoblastic leukemia (T-ALL) is a hematologic malignancy with a poor prognosis. It has been shown that long non-coding RNA (lncRNA) plays an important role in tumorigenesis. Here, we characterized a novel lncRNA, T-ALL-R-LncR1, with whole-transcriptome deep sequencing from the Jurkat leukemic T-cell line. T-ALL-R-LncR1 was not observed in human normal tissues. However, an obvious expression was observed in some tumor tissues. T-ALL-R-LncR1 was markedly expressed in neoplastic T lymphocytes of 11 cases out of 21 children with T-ALL, indicating that T-ALL-R-LncR1 might be associated with T-ALL. T-ALL-R-LncR1 knockdown predisposed Jurkat cells to undergo pro-apoptotic factor Par-4-induced apoptosis. Further studies revealed that T-ALL-R-LncR1 knockdown facilitated the formation of a Par-4/THAP1 protein complex, resulting in the activation of caspase-3 and an increase of pro-apoptotic Smac protein in T-ALL cells. Our studies indicate a potential role of suppressing the novel long non-coding RNA T-ALL-R-LncR1 in the therapy of human T-ALL. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 10428194
- Volume :
- 55
- Issue :
- 6
- Database :
- Academic Search Index
- Journal :
- Leukemia & Lymphoma
- Publication Type :
- Academic Journal
- Accession number :
- 96151223
- Full Text :
- https://doi.org/10.3109/10428194.2013.829574