2. Academic Validation
  3. The role of the novel LincRNA uc002jit.1 in NF-kB-mediated DNA damage repair in acute myeloid leukemia cells

The role of the novel LincRNA uc002jit.1 in NF-kB-mediated DNA damage repair in acute myeloid leukemia cells

  • Exp Cell Res. 2020 Jun 15;391(2):111985. doi: 10.1016/j.yexcr.2020.111985.
Ding Li 1,  Zelei Yu 2,  Tingting Wang 2,  Yi Li 3,  Xianling Chen 4,  Lixian Wu 5
Affiliations

Affiliations

  • 1 The Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, 450008, PR China; Department of Pharmacology, School of Pharmacy, Fujian Medical University, Fuzhou, 350108, PR China.
  • 2 Department of Pharmacology, School of Pharmacy, Fujian Medical University, Fuzhou, 350108, PR China.
  • 3 Department of Pharmaceutics, School of Pharmacy, China Pharmaceutical University, Nanjing, 210009, PR China.
  • 4 Fujian Institute of Hematology, Union Hospital, Fuzhou, 350001, PR China.
  • 5 Department of Pharmacology, School of Pharmacy, Fujian Medical University, Fuzhou, 350108, PR China; Institute of Materia Medicine, Fuzhou, 350108, PR China; Fuijan Key Laboratory of Natural Medicine Pharmacology, Fuzhou, 350108, PR China. Electronic address: wlx-lisa@126.com.
PMID: 32259522 DOI: 10.1016/j.yexcr.2020.111985
Abstract

The roles and therapeutic potential of long noncoding RNAs (lncRNAs) in acute myeloid leukemia (AML) have attracted increased attention. However, many lncRNAs have not been annotated in AML, and their predictive value for AML therapy remains unclear. In this study, we identified a novel large intergenic noncoding RNA uc002jit.1 (D43770) from a lncRNA microarray. We first proved uc002jit.1 is a target gene of nuclear factor kappa B/RELA, RELA regulated uc002jit.1 transcription by binding to its promoter. Additionally, uc002jit.1 knockdown impaired the stability of poly (ADP-ribose) polymerase 1 (PARP1) mRNA, and then reduced PARP1 protein content and PARylation level upon DNA damage, thus inhibiting DNA damage repair in AML cells. Moreover, uc002jit.1 knockdown significantly inhibited AML cells proliferation and increased the sensitivity to chemotherapeutic drugs in vitro as well as in a mouse model in vivo. Overall, our study indicated that uc002jit.1 may be associated with the occurrence and prognosis of AML and could be a new diagnostic/prognostic biomarker and therapeutic target for AML.

Keywords

AML; DNA damage Repair; NF-κB; PARP1; RELA; lincRNA; uc002jit.1.

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