PRL-3 Induces MiR-21 To Regulate PTEN Pseudogene PTENP1 In Endometrial Carcinoma

Objective: Endometrial cancer is one of the most common malignant tumors of female reproductive tract.In recent years,the incidence of endometrial cancer is on the rise all over the world.At present,endometrial cancer has become the second largest female reproductive system cancer after cervical cancer in China.It seriously affects women's physical and mental health.Endometrial carcinoma can be divided into estrogen dependent(type I)and non estrogen dependent(type II).It is believed that endometrial cancer is related to sustained high estrogen stimulation,oncogene activation and tumor suppressor gene inactivation.Based on the previous studies,this study further explored the molecular mechanism of PRL-3-mediated endometrial cancer.To explore the interaction among PRL-3,mi R-21 and PTENP1,and to provide a new idea for the treatment of endometrial cancer.Methods: 1.PRL-3 si RNA(small interference RNA)and,PRL-3 NC(PRL-3 si RNA negative control),mi R-21 mimic(mi R-21 analogue),mi R-21 NC(mi R-21 mimic negative control)were transfected in endometrial cancer cells HEC-1A by transient transfection,real-time RT-PCR detect the relative expression levels of PRL-3 m RNA and mi R-21 m RNA after transfection.2.Changes of mi R-21 and PTNP1 after transfection of PRL-3 si RNA and PRL-3 NC.3.Change of PTENP1 after transfection of mi R-21 mimic and mi R-21 NC.Results: 1.Compared with the negative control group,the relative expression of PRL-3 m RNA in the interference group decreased(P<0.05 ***),and the relative expression of mi R-21 m RNA in the transfection group increased(P < 0.05 *).2.The relative expression of mi R-21 m RNA and PTENP1 m RNA decreased and increased after interfering with PRL-3 si RNA(P < 0.05 *).3.The relative expression of PTENP1 m RNA decreased after mi R-21 mimic was transfected(P < 0.05 *).Conclusion: PRL-3 can down regulate the expression of PTENP1 by up regulating mi R-21 in endometrial carcinoma.