Y2007C053, 2009ZRB14176 and ZR2016HQ46), Technology Development Projects of Shandong Province (grant nos. partly attenuated by treatment with IL-4. Inhibition of miR-155 expression significantly increased cell apoptosis despite the presence of IL-4. The results of the present study suggested that treatment with IL-4 enhanced the expression of miR-155, which regulated CLL cell survival via the enhanced phosphorylation of STAT6. (23). In the present study, the results exhibited that a novel signaling pathway, the p-STAT6-mediated extracellular IL-4 upregulation of Klf2 miR-155, is usually involved in CLL pathology. IL-4-driven alternative macrophage activation and proliferation are characteristic features of anti-helminthic immune responses, which primarily occur during inflammatory responses (23,24). The signaling pathways associated with genome-wide miRNA expression and cellular functions regulated by miRNAs during alternative macrophage activation remain largely unknown. Numerous studies have investigated the functions of IL-4-regulated miRNAs in human and mouse alternative macrophage activation (25C27). Furthermore, ~1,000 miRNAs are present in the human genome; however, little is known about the transcriptional regulation of miRNAs (28,29). Considering that miRNA expression levels are deregulated in CLL, the present study aimed to determine whether STAT6 affected the transcription levels of miRNAs in CLL cells (30,31). Our previous study indicated that following treatment with rIL-4, levels of p-STAT6 in MEC-1 cells increased in a time-dependent manner (17). Based on these data, the present study aimed to determine whether miR-155 was involved in the development of CLL. The results exhibited that pretreatment with rIL-4 promoted the expression of miR-155; however, this effect was attenuated following transfection with siSTAT6. These results suggested that rIL-4 induced the expression of miR-155 via STAT6 phosphorylation. The effects of miR-155 were decided to additionally investigate the function of miR-155 in CLL pathogenesis. The results revealed that miR-155 decreased apoptosis levels in MEC-1 cells, which suggested that this upregulation of miR-155 may be associated with the pathogenesis of CLL. In conclusion, the results of the present study exhibited that IL-4 induced miR-155 expression and STAT6 phosphorylation. STAT6 knockdown was revealed to suppress IL-4-induced miR-155 expression. Overexpression of miR-155 was demonstrated to decrease the apoptotic rate of MEC-1 cells; whereas overexpression of anti-miR-155 was demonstrated to enhance MEC-1 cell apoptosis. The results of the present study suggested that miR-155 expression was induced by IL-4, which subsequently enhanced p-STAT6 levels to regulate CLL cell survival. The results of the present study have provided an improved understanding regarding the MK-0752 molecular mechanism of CLL pathogenesis and identified a novel therapeutic target for the treatment of patients with CLL. Acknowledgements Not applicable. Funding The present MK-0752 study was partly supported by the National Natural Science Foundation (grant nos. 81500124 and 81600121), Natural Science Foundations of Shandong Province (grant nos. Y2007C053, 2009ZRB14176 and ZR2016HQ46), Technology Development Projects of Shandong Province (grant nos. 2007GG10 and 2010GSF10250), Major Research Projects of Shandong Province (grant nos. MK-0752 2016GSF201029 and 2017GSF218007), Program of Shandong Medical MK-0752 Leading Talent and Taishan Scholar Foundation of Shandong Province. Availability of MK-0752 data and materials The analyzed data sets generated during the study are available from the corresponding author upon affordable request. Authors’ contributions NC and XW conceived and designed the study. NC, LF, KL, XL and PL performed the experiments. NC and XL wrote the paper. NC, PL and XW reviewed and edited the manuscript. All authors read and approved the manuscript and agree to be accountable for all aspects of the research in ensuring that.