| Background: Leukemia is a common hematological malignant disease of hematopoietic stem or progenitor cells.Abnormal cloning of leukemia cells causes uncontrolled cell proliferation,blocked differentiation,blocked apoptosis,and aggregation in bone marrow and other non-hematopoietic tissues,thus inhibiting normal hematopoietic and immune function.Urinary thelial cancer associated 1(UCA 1)was first identified in bladder cancer by using high-throughput RNA sequencing,whose expression is abnormal in bladder cancer and is associated with its poor prognosis.Lnc RNA UCA1 has been shown to be highly expressed in multiple human tumors,however the mechanism of Lnc RNA UCA1 in acute myeloid leukemia is not well defined.Objective: To explore the expression of long noncoding RNA UCA1 in acute myeloid leukemia(AML),and observe the effects of Lnc RNA UCA1 on the proliferation,apoptosis and Wnt pathway in acute myeloid leukemia cells.Methods: We collected 30 bone marrow samples from AML patients and 30 patients of iron deficiency anemia first diagnosed in the Hematology Department of the First Affiliated Hospital of Bengbu Medical College from May 2019 to December 2019,and the expression level of Lnc RNA UCA1 in AML bone marrow was quantified by real-time PCR(q RT-PCR).AML cells were divided into three groups: UCA1-si RNA,untransfected control(NC)and blank plasmid vector(Vector).The expression levels of Lnc RNA UCA1 in the cells were determined by q RT-PCR.The proliferation of AML cells was determined by MTT.AML apoptosis was measured by flow cytometry;Western blot measured the levels of Wnt pathway-related proteins Wnt,β-catenin,and p-gsk-3 β in AML cells.Results: The expression level of Lnc RNA UCA1 was significantly higher in AML tissues and cells than in anemia patient tissues and human bone marrow stromal cells(P<0.01).Compared with the Vector and NC groups,the UCA1 level was significantly reduced in the AML cells of the UCA1-si RNA group(P <0.05),the cell proliferation rate was significantly low(P <0.05),the expression levels of Wnt and β-catenin proteins were significantly decreased;the expression level of p-gk-3β protein significantly increased,there was no significant difference between AML indicators in Vector and NC groups(P> 0.05).Conclusion: Knockdown of Lnc RNA UCA1 in AML cells inhibited cell proliferation and promoted apoptosis,and the mechanism may be related that knockdown of UCA 1can inhibit Wnt signaling pathway. |