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Acute myeloid leukemia (AML) is a highly heterogeneous disease featured by a clonal proliferation derived from primitive hematopoietic stem/progenitor cells. Circular RNAs (circRNAs) have been identified as crucial regulators in the progression of various cancers, including AML. However, the molecular mechanism of AML is still not definite. This study aimed to explore the influences of circ_0012152 on cell development in AML cells and the underlying regulatory mechanism. The expression of circ_0012152, microRNA-625-5p (miR-625-5p) and sex-determining region Y-related high mobility group box 12 (SOX12) was detected by quantitative real-time polymerase chain reaction. The proliferation of AML cells was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay for cell viability, 5-ethynyl-2'-deoxyuridine incorporation assay for DNA biosynthesis and flow cytometry for cell cycle distribution, respectively. The death of AML cells was detected by flow cytometry. The protein expression was assessed by Western blot assay. Dual-luciferase reporter and RNA immunoprecipitation assays were carried out to examine the relationships among circ_0012152, miR-625-5p and SOX12. The expression of circ_0012152 was increased in AML tissues and cells and circ_0012152 knockdown suppressed proliferation and promoted death in AML cells. Further exploration revealed that circ_0012152 inhibited miR-625-5p expression and downregulation of miR-625-5p overturned the effects of circ_0012152 knockdown on proliferation and death in AML cells. Moreover, miR-625-5p targeted SOX12 and circ_0012152 facilitated the expression of SOX12 by relieving miR-625-5p-mediated inhibitory effect on SOX12 in AML cells. Circ_0012152 knockdown suppressed cell proliferation and promoted death by targeting SOX12 mediated by miR-625-5p in AML cells.

Glucocorticoids (GC) are used as the first-line treatment of immune thrombocytopenia (ITP), but 10-20% of patients are insensitive to them. Regulatory T cells (Tregs) can maintain immune tolerance in autoimmune diseases. The present research pooled 55 patients with newly diagnosed ITP and 44 healthy volunteers from seven hospitals. All patients received GC treatment and were divided into GC-sensitive and GC-insensitive groups according to the curative effect after 2 weeks of treatment. The levels of lymphocyte subgroups and Tregs were recorded. As the results indicated, the levels of CD8+ CD25str+ Tregs in the GC-sensitive group were significantly higher than that of the GC-insensitive group (P = 0·005). The optimal critical value of CD8+ CD25str+ Tregs to distinguish GC sensitivity was 0·09%. With GC therapy the level of CD45RO+ /CD8+ CD25str+ Tregs (activated type) decreased after treatment (P = 0·02) and the level of CD45RO- /CD8+ CD25str+ Tregs (initial type) increased slightly (P = 0·11). There were no obvious changes in the level of CD4+ Tregs. These findings support that the level of CD8+ CD25str+ Tregs and its subgroups have a predictive value in judging the sensitivity to GC among patients with ITP. Trial registration: www.chictr.org.cn; ChiCTR-OON-17014165.