Background LncRNAs play an important role in tumorigenesis and development in tumors, but the function of lncRNA SOCS2-AS in acute myeloid leukemia (AML) is unknown. in MV4-11 cells. The miR-221 shows overexpression in FLT3-ITD+ AML patients compared to FLT3-ITD- AML patients. And the expression level of miR-221 and SOCS2-AS displays negative relationship in FLT3-ITD+ AML individuals. Functionally, SOCS2-AS could possibly be interacted with miR-221 in AML cells. After SOCS2-AS knockdown, the phosphorylation degree of STAT5 was reduced. Furthermore, miR-221 inhibitor can save the viability in cells after si-SOCS2-AS transfection. Which is mentioned that SOCS2-AS regulates the STAT5 sign transduction pathway with sponging URB597 inhibition miR-221. Summary In conclusion, this scholarly research confirms the molecular mechanism of SOCS2-AS in AML by focusing on the miR-221/STAT5 signaling pathway. This means that SOCS2-AS might serve as a potential therapeutic target for the treating AML. strong course=”kwd-title” Keywords: SOCS2-AS, severe myeloid leukemia, miR-221, FLT3-ITD+ Intro Severe myeloid leukemia (AML) can be a malignant hematological disease due to uncontrolled proliferation, clogged dysdifferentiation and apoptosis of bone tissue marrow hematopoietic stem cells.1 The mutation of FMS-like receptor tyrosine kinase 3 (FLT3) happens in about 1/3 of individuals with severe myeloid leukemia, and its own inner tandem mutation (ITD) often qualified prospects to fast disease development and poor prognosis.2,3 To boost the prognosis of FLT3-ITD+individuals, many FLT3 inhibitors have already been posted, but these drugs possess limited efficacy. The recurrence price of individuals treated with solitary drug is near 100%.4 Therefore, it really is urgent to help expand research the molecular system of URB597 inhibition FLT3-ITD+ mutant leukemia for the treating AML. Long non-coding RNA (LncRNA) can be a kind of RNA with molecular pounds higher than 200 b, and can’t be translated into proteins, but could be used like a molecular sponge to modify gene expression by binding to miRNAs, thereby affecting gene expression.5,6 More and more studies have found that LncRNA plays an important physiological and pathological role in tumorigenesis and development.7 It is not only widely involved in promoting tumorigenesis and development in solid tumors, but also reported to be of great significance in hematological tumors.8 It is reported that LINC00152 regulated the expression of CDK9 by combining with miR-193a and promoted the occurrence and development of AML.9 Inhibiting LncRNA MALAT1 could promote DNA damage and apoptosis in multiple myeloma cells, thereby inhibiting tumor growth.10 Suppressor of cytokine signaling-2, as one of LncRNAs, was exhibited that it is related to AML progression.11 Laszlo et al reported that higher SOCS2 expression would have a poor outcome in pediatric acute myeloid leukemia.12 Therefore, exploring the role of SOCS2 in AML will contribute to reveal the molecular mechanism, and provide therapeutic targets for AML treatment. In this study, it is found that the ectopic expression SYK of SOCS2-AS in FLT3-ITD + leukemia and overexpression SOCS2-AS promote cell proliferation and colony formation, repress apoptosis in FLT3-ITD + cell lines. Mechanically, it is exhibited that SOCS2-AS promotes cell proliferation by regulating STAT5 through miR-221. Materials and Methods Clinical Samples The clinical samples were collected from Xian Gaoxin Hospital. The research was approved by Ethics Committee of Xian Gaoxin Hospital and written informed consents were obtained from the patients (Clinical trial registration number: CTR20191008). Seventy-one FLT3-ITD+ AML patients, 287 FLT3-ITD- AML patients URB597 inhibition and 330 healthy donors were enrolled and the bone marrow samples were collected. Obtained samples were quickly frozen at ?80C for storage. All URB597 inhibition the patients were newly diagnosed. Initial AML patients were alleviated by anthracycline plus cytarabine, while M3 sufferers were treated with all-trans retinoic arsenic or acidity. The clinicopathological features had been list in Desk 1. Desk 1.