Inhibition of Lnc-OC1 Induced Cell Apoptosis and Decreased Cell Viability by Releasing miR-34a and Inhibiting PD-L1 in Endometrial Carcinoma.

Abstract

Now, there is a growing awareness of the role to long non-coding RNAs (lncRNAs) in tumorigenesis and progression of a variety of malignancies including endometrial carcinoma (EC). Here, we explored the potential molecular mechanism of Lnc-OC1, a novel lncRNA, in the development of EC. Our results suggested that Lnc-OC1 was significantly upregulated in EC tissues comparing with normal tissues. Besides, Lnc-OC1 was higher expressed in the more advanced stage of EC. Therefore, Lnc-OC1 might be a crucial regulator in the progress of EC. Moreover, knockdown of Lnc-OC1 leaded to an inhibition of cell viability and a raise of cell apoptosis. In addition, Lnc-OC1 could sponge miR-34a and thus decrease its expression. miR-34a was proved to be a tumor suppressor in different malignance, hence downregulating Lnc-OC1 helped to alleviate EC by releasing miR-34a. Furthermore, rescue experiments significantly indicated that knockdown of Lnc-OC1 inhibited cell growth through repressing PD-L1 expression at least partially. Concisely, our results proved that Lnc-OC1/miR-34a/PD-L1 axis might serve as a therapeutic target of EC.