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Retracted : LINC00449 regulates the proliferation and invasion of acute monocytic leukemia and predicts favorable prognosis
Author(s) -
Shi Yuan,
Zhu Yuandong,
Zheng Xiao,
Zheng Zhuojun
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29487
Subject(s) - myeloid leukemia , long non coding rna , biology , cancer research , in vivo , cell growth , rna , competing endogenous rna , microrna , leukemia , in vitro , microbiology and biotechnology , gene , immunology , biochemistry , genetics
Acute myeloid leukemia (AML) is a highly aggressive disease that causes high mortality. Long noncoding RNA (lncRNA) have studied in recent years that could be a potential biomarker and therapeutic target. Therefore, it is urgently necessary to explore the novel lncRNAs in AML. Microarray analysis was performed to determine the differentially expressed lncRNAs between mononuclear cells of AML and normal samples. The biological function of lncRNA on cell proliferation and migration was measured in vitro. The predicted downstream target of lncRNA was validated by dual‐luciferase reporter assay, RNA immunoprecipitation, RNA pull‐down, and rescue experiments. The tumor formation and metastasis study were conducted in vivo. The expression of lncRNA in clinical samples was determined by a quantitative reverse transcription‐polymerase chain reaction. LINC00449 was one of the most differentially expressed lncRNA which is mainly located in the cytoplasm. We found that overexpression of LINC00449 could inhibit the cell proliferation and invasion of AML cells in vitro and in vivo. Besides, miR‐150 was identified as the downstream target gene that was negatively regulated by LINC00449 and FOXD3 was targeted by miR‐150. The results were confirmed by dual‐luciferase reporter assay, RNA immunoprecipitation, RNA pull‐down, rescue experiments, and in vivo assays. Patients with AML with high expression of LINC0049 may characterize a favorable survival. All the above‐mentioned findings indicated that the LINC00449/miR‐150/FOXD3 signaling pathway might represent a novel prognostic biomarker or therapeutic target for the treatment of AML.