| Objective: 1.To study the expression and significance of LUCAT1 in endometrial carcinoma.2.To study the effects of UPF 1 combined with LUCAT1 on the proliferation,migration,invasion,cycle and other biological behaviors of type Ⅰ endometrial cancer cells.3.To observe the regulatory effect of LUCAT1 on PI3K/ Akt pathway protein of endometrial cancer cells;4.To observe the effect of UPF 1 combined with LUCAT1 on the growth rate of transplanted tumor in nude mice in vivo.5.To investigate the mechanism of UPF1 regulation of LUCAT1 on the biological behavior of type Ⅰ endometrial cancer cells.Materials and Methods: 1.Endometrial carcinoma tissues were collected from 31 patients admitted to Shengjing Hospital of China Medical University and diagnosed as endometrial adenocarcinoma by pathological examination from March 2017 to October2018,and the expression level of LUCAT1 was detected by real-time quantitative PCR.The relationship between the clinical and pathological data was analyzed.2.LUCAT1 overexpressed plasmid and blank control were transfected in type Ⅰ endometrial cancer cell lines,and si RNA interfered with Lucat1 and blank control;CCK-8,scratch assay,Transwell assay and cell cycle assay were performed to verify the effect of LUCAT1 on the function of endometrial cancer cells.3.RNA immune precipitation(RIP)verified the specific binding of Luc AT1 to UPF1.The stability experiment verified the influence of UPF1 on the stability of LUCAT1.4.After overexpression and knockdown of LUCAT1,the expression of PI3K/ Akt pathway-related proteins was verified by Western blot.5.Rescue experiments were performed to silence Lucat1 while overexpression of UPF1,and CCK8,scratch test,Transwell test,and cell cycle test were performed after knockdown of UPF1 and overexpression of Lucat1.6.In nude mice,the effects of UPF 1 combined with Lucat 1 on the growth rate of transplanted tumor in vivo and the changes in the expression of PI3K/ Akt pathway related proteins were verified.Results: 1.The expression of LUCAT1 was high in endometrial cancer tissues and correlated with clinical stage.Compared with early and late stage patients,the later the stage,the higher the LUCAT1 was.2.Overexpression of LUCAT1 can promote the proliferation,migration and invasion of endometrial cancer cells,and the cells enter the division phase,and the cells decrease in the G0-G1 phase.Silencing LUCAT1 can inhibit the proliferation,migration and invasion of endometrial cancer cells,and the cells are arrested in G0-G1 phase.3.UPF1 can bind to LUCAT1 in endometrial cancer cells,and overexpression of UPF1 promotes the stability of LUCAT1.4.Salvage experiments showed that LUCAT1 could rescue the biological behavior of endometrial cancer cells caused by UPF1 silencing/overexpression.5.Western experiments showed that Luc AT1 overexpression could activate the PI3K/ Akt pathway,and LUCAT1 silencing could inhibit the PI3K/ Akt pathway.6.Experiments in nude mice showed that in vivo silencing of UPF1 could reduce the growth rate of xenograft tumor in nude mice,Lucat1 could partially recover the tumor suppressant effect induced by UPF1 silencing,and the ratio of p-Akt/Akt also changed accordingly.Conclusion: 1.This study found that UPF1 and LUCAT1 were highly expressed in endometrial carcinoma tissues and correlated with clinical staging.2.UPF 1 combined with Lucat 1 affects the proliferation,migration,invasion,cycle and other biological behaviors of endometrial cancer cells.3.LUCAT1 can regulate the PI3K/ Akt pathway protein of endometrial cancer cells.4.UPF 1 combined with LUCAT 1 affects the growth rate of transplanted tumor in nude mice in vivo.5.UPF1-LUCAT1-PI3K/Akt regulatory axis plays an important role in the malignant progression of type Ⅰ endometrial carcinoma... |
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