Open AccessInteraction between LncRNA-ROR and miR-145 contributes to epithelial-mesenchymal transition of ovarian cancer cells
Author(s) -
Jie Li,
Songlin Zhang,
Lei Wu,
Meili Pei
Publication year - 2019
Publication title -
general physiology and biophysics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.376
H-Index - 39
eISSN - 1338-4325
pISSN - 0231-5882
DOI - 10.4149/gpb_2019028
Subject(s) - ovarian cancer , epithelial–mesenchymal transition , cancer research , reprogramming , biology , competing endogenous rna , cancer , microrna , long non coding rna , transition (genetics) , cell , gene , rna , genetics
Emerging evidence has indicated that long noncoding RNAs (LncRNAs) play critical roles in tumor development. LncRNA-regulator of reprogramming (ROR) could enhance the malignance of numerous tumors through promoting cell reprogramming and the chemoresistance of several cancers. Nevertheless, the detailed molecular mechanisms of LncRNA-ROR in ovarian cancer are not well elucidated. In our study, we demonstrated that LncRNA-ROR was high expression in ovarian cancer tissues than in normal ovarian tissues, and LncRNA-ROR level was positively associated with clinical stages and the differentiation grades of malignant cells. Functionally, LncRNA-ROR could induce epithelial-mesenchymal transition (EMT), and regulated ovarian cancer cell migration and invasion by decreasing the expression of tumor suppressive miR-145 and its target gene FLNB. Moreover, the binding site for miR-145 within LncRNA-ROR contributed to the reciprocal negative regulation of LncRNA-ROR and miR-145. Taken together, LncRNA-ROR promoted EMT by the miR-145/FLNB regulatory axis in ovarian cancer, providing a potential therapeutic target for ovarian cancer.