2. Academic Validation
  3. LncRNA CD27-AS1 promotes acute myeloid leukemia progression through the miR-224-5p/PBX3 signaling circuit

LncRNA CD27-AS1 promotes acute myeloid leukemia progression through the miR-224-5p/PBX3 signaling circuit

  • Cell Death Dis. 2021 May 18;12(6):510. doi: 10.1038/s41419-021-03767-9.
Yanling Tao 1,  Jingjing Zhang 2 3,  Lulu Chen 2 3 4,  Xin Liu 2 3 4,  Mingkang Yao 2 3 4,  Hao Zhang 5 6
Affiliations

Affiliations

  • 1 Department of Pediatric Hematology, Affiliated Hospital of Jining Medical University, Jining, Shandong Province, China.
  • 2 Department of Hematology, Affiliated Hospital of Jining Medical University, Jining, Shandong Province, China.
  • 3 Institute of Blood and Marrow Transplantation, Jining Medical University, Jining, Shandong Province, China.
  • 4 Graduate School, Department of Clinical Medicine, Jining Medical University, Jining, Shandong Province, China.
  • 5 Department of Hematology, Affiliated Hospital of Jining Medical University, Jining, Shandong Province, China. [email protected].
  • 6 Institute of Blood and Marrow Transplantation, Jining Medical University, Jining, Shandong Province, China. [email protected].
PMID: 34006845 DOI: 10.1038/s41419-021-03767-9
Abstract

Acute myeloid leukemia (AML) is a hematological malignancy with a low cure rate, especially in the elderly. Previous studies have shown that long non-coding RNA (lncRNA) may be an important factor in the pathogenesis of hematological malignancies, including acute myeloid leukemia (AML). However, the biological roles and clinical significances of most lncRNAs in AML are not fully understood. LncRNA CD27 Antisense RNA 1 (CD27-AS1), as a member of lncRNA family, has rare reports on its function. In present study, we found that the expression of CD27-AS1 examined by quantitative Real-Time PCR was markedly increased in the AML patients (N = 40) compared with healthy volunteers (N = 40). The overall survival time was significantly shorter in patients with higher CD27-AS1 expression than that in patients with lower CD27-AS1 (P < 0.01). Furthermore, downregulation of CD27-AS1 in AML cells suppressed proliferative ability, arrested cell cycle in G0/G1 phase, and induced Apoptosis. However, CD27-AS1 overexpression further enhanced the malignant phenotype of AML cells. Additionally, CD27-AS1 was proved to increase PBX3 expression through sponging miR-224-5p. CD27-AS1 knockdown blocked the MAPK signaling through PBX3 silencing and further inhibited the cell growth of AML cells. Taken together, we demonstrate that CD27-AS1 may be a potential prognostic biomarker of AML, and our finding also provides a new insight for non-coding RNA-based therapeutic intervention of AML.

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