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

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.

Keywords::

• Long non-coding RNA
• Par-4
• apoptosis
• T cell
• leukemia

Potential conflict of interest

Disclosure forms provided by the authors are available with the full text of this article at www.informahealthcare.com/lal.

This work was supported by the National Natural Science Foundation of China (81170487, 81170661, 81270613, 81170485).