Effect Of LncRNA TUG1 On The Biological Characteristics Of Endometrial Cancer By Regulating MiR-181a-5p/NOTCH2

BackgroundEndometrial cancer is a common malignant tumor in the clinic,and its pathogenesis has not been fully elucidated.Several studies have shown that LncRNA-miRNA-m RNA plays an important regulatory role in the development of endometrial cancer.Long-chain non-coding RNA Taurine up-regulated gene 1(LncRNA TUG1)may play an oncogene role in the development of endometrial cancer.Bioinformatics analysis revealed that micro RNA-18 1a-5p(miR-181a-5p)may be a target gene of TUG1,and Notch receptor 2(NOTCH2)may be a target gene of miR-181a-5p.So we propose whether LncRNA TUG1 affects the biological behavior of endometrial cancer cells by regulating the miR-181a-5p/NOTCH2.PurposeTo explore the effect of LncRNA TUG1 on the biological characteristics of endometrial cancer by regulating miR-181a-5p/NOTCH2.It provides a new way for clinical targeted treatment of endometrial cancer.Part I si-TUG1 Inhibits the Growth of Endometrial Cancer Cells Methods1.The expression level of TUG1 in endometrial cancer tissues and cell lines was detected by real-time fluorescent quantitative polymerase chain reaction(qRT-PCR).2.The clinical and pathological data of 56 patients with endometrial cancer were collected and followed up for 5 years.The relationship between TUG1 expression and clinicopathological features was compared,and the relationship between TUG1 expression and prognosis was analyzed by Kaplan-Meier method.3.Endometrial cancer JEC,HEC-1B,RL952,Ishikawa cells and endometrial epithelial HEECs were cultured in vitro,and si-NC and si-TUG1 were transfected into endometrial cancer HEC-1B,RL952 cells by lipofection,using cell methylthiazolyl tetrazolium(MTT)assay to detect cell proliferation.Transwell assays detect cell migration and invasion.Results1.The expression level of TUG1 in endometrial carcinoma tissues and cell lines was significantly increased(P<0.05).2.The high expression of TUG1 was positively correlated with the degree of differentiation,clinical stage,lymph node metastasis and myometrial invasion(P<0.05).The survival rate of TUG1 high expression group was significantly lower than that of low expression group(P<0.05).3.The cell proliferation ability was significantly decreased after silencing TUG1 expression(P <0.05),and the number of migration and invasion cells was significantly decreased(P <0.05).Conclusion:TUG1 can promote the malignant progression of endometrial cancer.Part II Mechanism of TUG1 Regulating Growth of Endometrial Carcinoma Cells via miR-181a-5p/NOTCH2 Methods1.The dual luciferase reporter assay and RIP assay were used to verify the targeting relationship between TUG1 and miR-181a-5p.qRT-PCR was used to detect the expression of miR-181a-5p in endometrial carcinoma tissues and different cell lines.The proliferation,migration and invasion ability of each group of cells were examined.2.The dual-luciferase reporter assay and RIP assay were used to verify the targeted binding relationship between miR-181a-5p and NOTCH2.The expression of NOTCH2 in endometrial carcinoma tissues and cell lines was detected by qRT-PCR.Western blot analysis was used to detect the regulatory relationship between NOTCH2,TUG1 and miR-181a-5p.Results1.Dual fluorescent reporter gene assay and RIP assay demonstrated that miR-181a-5p is the target gene of TUG1.The expression level of miR-181a-5p was significantly decreased in endometrial carcinoma tissues and cell lines(P<0.05).Overexpression of miR-181a-5p inhibited proliferation,migration and invasion of endometrial cancer cells(P<0.05).2.Dual luciferase reporter assay and RIP assay demonstrated that NOTCH2 is the target gene of miR-181a-5p.The expression level of NOTCH2 in endometrial cancer tissues and cell lines was significantly increased(P <0.05).The expression level of miR-181a-5p in si-TUG1 group was significantly increased.The expression of NOTCH2 in cells was significantly increased after co-transfection of si-TUG1 and anti-miR-181a-5p(P <0.05).Conclusion:TUG1 can promote the malignant progression of endometrial cancer by regulating the miR-181a-5p /NOTCH2.