Objective To investigate the proportion of CD_4~+ CD_(25)~+ Tregs in the peripheral blood of the patients suffering from acute myeloid leukemia (AML) with or without chemotherapy and clinical significance.Methods The flow cytometry was used to evaluate the proportion of CD_4~+ CD_(25)~+ CD_(127)~(low) T cells in the peripheral blood of the patients with primary AML group (group A), AML who achieved complete remission over 3 years (group C) or less than 3 years(group B) and the healthy donors. Results The percentages of CD_4~+ CD_(25)~+ Tregs of group A and B was significantly higher than that of control group (P <0.05); but not significantly defferent among the group C and control group (P >0.05). The percentages of CD_4~+ CD_(25)~+ Tregs of group A was significantly higher than that of group B and C. Conclusion These results suggested that CD_4~+ CD_(25)~+ Tregs played an important role in acute myeloid leukemia.

OBJECTIVE: To explore the effect of HNF1A-AS1 on the proliferation, migration and invasion of IL-6-induced hemangioendothelial cells (HemEC) and possible mechanism. METHODS: RT-qPCR was used to detect the expression level of HNF1A-AS1 and miR-363-3p in the tumor tissue and adjacent normal skin tissue from 35 patients with hemangioma. Pearson correlation was used to analyze the correlation between the expression of HNF1A-AS1 and miR-363-3p in tumor tissues. HemEC were isolated and cultured in vitro.Dual luciferase reporter gene experiment was used to study the regulatory effect between HNF1A-AS1 and miR-363-3p. IL-6 was added to HemEC transfected with si-NC, si-HNF1A-AS1, si-HNF1A-AS1 and anti-miR-NC, or si-HNF1A-AS1 and anti-miR-363-3p, respectively. CCK-8 method and clone formation experiment were used to detect cell proliferation in each group. Transwell method was used to detect cell migration and invasion in each group. Western blotting was used to detect the expression of Ki67, MMP-2 and MMP-9 proteins in each group. RESULTS: Compared with normal skin tissues, the expression of IL-6 mRNA in hemangioma tissues was increased (P<0.05), and the expression of IL-6 mRNA in the proliferative phase was lower than that in the degenerative phase (P<0.05). Expression of HNF1A-AS1 in hemangioma tissue was increased (P<0.05), while that of miR-363-3p was decreased (P<0.05), and the two were negatively correlated (r=-0.758, P<0.05). HNF1A-AS1 down-regulated the expression of miR-363-3p in HemEC.IL-6 promoted the expression of HNF1A-AS1, OD value, number of colonies, number of migration and invasion of HemEC cells, and the expression of Ki67, MMP-2 and MMP-9proteins (P<0.05), while reduced the expression of miR-363-3p (P<0.05). Down-regulating si-HNF1A-AS1 reduced the IL-6-induced HemEC cell OD value, colony numbers, migration and invasion and the expression of Ki67, MMP-2 and MMP-9 proteins (P<0.05). Down-regulating miR-363-3p attenuated the inhibitory effect of down-regulating si-HNF1A-AS1 on the proliferation, migration and invasion of HemEC cells induced by IL-6 (P<0.05). CONCLUSION Expression of HNF1A-AS1 is increased in hemangioma tissues. Down-regulating HNF1A-AS1 may inhibit proliferation, migration and invasion of IL-6-induced hemangioma endothelial cells by targeted up-regulation of miR-363-3p.
Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Endothelial Cells ; Gene Expression Regulation, Neoplastic ; Hemangioma/genetics* ; Hepatocyte Nuclear Factor 1-alpha/genetics* ; Humans ; Interleukin-6/genetics* ; MicroRNAs/genetics* ; RNA, Long Noncoding