Knockdown of ADORA2A antisense RNA 1 inhibits cell proliferation and enhances imatinib sensitivity in chronic myeloid leukemia.

Yabo Liu, Huibo Li, Yanqiu Zhao, Dandan Li, Qian Zhang, Jinyue Fu, Shengjin Fan
Author Information
  1. Yabo Liu: Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
  2. Huibo Li: Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
  3. Yanqiu Zhao: Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
  4. Dandan Li: Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
  5. Qian Zhang: Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
  6. Jinyue Fu: Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.
  7. Shengjin Fan: Department of Hematology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. ORCID

Abstract

Long non-coding RNAs (LncRNAs) exert important regulatory roles in chronic myeloid leukemia (CML). In this study, we aimed to investigate the potential role and molecular mechanism of lncRNA ADORA2A antisense RNA 1 (ADORA2A-AS1) in CML. We found that the expression of ADORA2A-AS1 was upregulated in CML. Further, knockdown of ADORA2A-AS1 inhibited the proliferation, induced apoptosis, arrested cell cycle, and enhanced imatinib sensitivity in CML cells. Besides, ADORA2A-AS1 promoted the expression of transforming growth factor-beta receptor 1 (TGFBR1) and ATP binding cassette subfamily C member 2 (ABCC2) via sponging miR-665, thereby exerting a tumor-promoting activity. Collectively, our results confirmed the oncogenic effect of ADORA2A-AS1 in CML, indicating that ADORA2A-AS1 is a promosing therapeutic target for CML.

Keywords

References

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MeSH Term

Adult
Cell Proliferation
Drug Resistance, Neoplasm
Female
Gene Knockdown Techniques
HEK293 Cells
Humans
Imatinib Mesylate
K562 Cells
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Male
Middle Aged
RNA, Antisense
RNA, Neoplasm

Chemicals

RNA, Antisense
RNA, Neoplasm
Imatinib Mesylate

Word Cloud

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