z-logo
Premium
Hsa_circ_0002483 regulates miR‐758‐3p/MYC axis to promote acute myeloid leukemia progression
Author(s) -
Xiao Yi,
Ming Xi,
Wu Jiaying
Publication year - 2021
Publication title -
hematological oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 44
eISSN - 1099-1069
pISSN - 0278-0232
DOI - 10.1002/hon.2829
Subject(s) - cell cycle , myeloid leukemia , cancer research , cell growth , apoptosis , microrna , flow cytometry , oncogene , gene knockdown , cell cycle checkpoint , leukemia , chemistry , biology , microbiology and biotechnology , immunology , gene , biochemistry
Circular RNAs are relevant to progression of acute myeloid leukemia (AML). Nevertheless, how and whether hsa_circ_0002483 (circ_0002483) participates in AML progression are largely uncertain. The bone marrow samples were harvested from 31 AML patients or 31 normal subjects. Circ_0002483, microRNA (miR)‐758‐3p and myelocytomatosis oncogene (MYC) abundances were examined via quantitative reverse transcription polymerase chain reaction and Western blot. Cell proliferation, cycle process and apoptosis were analyzed via Cell Counting Kit‐8, flow cytometry, caspase 3 activity and related protein levels. Target relationship was investigated by dual‐luciferase reporter assay and RNA immunoprecipitation. Circ_0002483 expression was elevated in AML patients and cells. Circ_0002483 silence constrained AML cell proliferation and facilitated cell cycle arrest and apoptosis. miR‐758‐3p was reduced in AML and decreased via circ_0002483. miR‐758‐3p down‐regulation mitigated the inhibitive influence of circ_0002483 interference on AML progression. MYC was decreased by miR‐758‐3p, and circ_0002483 could regulate MYC expression by miR‐758‐3p. miR‐758‐3p overexpression restrained cell proliferation and promoted cycle arrest and apoptosis via decreasing MYC. Circ_0002483 knockdown repressed AML cell proliferation and promoted cycle arrest and apoptosis via controlling miR‐758‐3p/MYC axis.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here