Objective To preliminarily explore the mechanism histone demethylase KDM5A in regulating the occurrence and development of acute myeloid leukemia (AML) through long non-coding RNA (LncRNA) TRIM52-AS1.
Methods The levels of KDM5A and TRIM52-AS1 were detected by real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot in the serum and various leukemia cells of AML patients. The targeting relationship between KDM5A and TRIM52-AS1 was detected by dual luciferase reporter assay. The effects of KDM5A and TRIM52-AS1 on HL-60 cell proliferation were detected by CCK8 assay. The effects ofKDM5A and TRIM52-AS1 on HL-60 cell migration were detected by Transwell assay.
Results KDM5A was highly expressed in the serum and various leukemia cells of AML patients, while TRIM52-AS1 was lowly expressed (P < 0.05). KDM5A could targetedly inhibit TRIM52-AS1. Overexpression of TRIM52-AS1 could targetedly inhibit leukemia cell proliferation and migration, and KDM5A could inhibit leukemia cell proliferation and migration by inhibiting TRIM52-AS1 (P < 0.05).
Conclusion Histone demethylase KDM5A can inhibit the occurrence and developmen of AML by inhibiting LncRNA TRIM52-AS1.