Y-L Hu1, Y-X Zhang, N Liu, H Liu, Y-C Yuan. 1. Department of Mother and Baby Health Paradise, People's Hospital of Rizhao, Rizhao, China. x6g0h6@163.com.
Abstract
OBJECTIVE: The long non-coding RNA MIR503 host gene (MIR503HG) plays a role in suppressing or promoting cancer in many types of human malignant tumors. The role of MIR503HG in cervical cancer is still unknown. PATIENTS AND METHODS: The expression level of MIR503HG in cervical cancer tissues and cell lines was accessed using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay. The Cell Counting Kit-8 (CCK-8) assay and flow cytometric analysis were performed to assess cell proliferation and apoptosis in cervical cancer. The nude mouse xenograft experiment was used to examine the ability of MIR503HG in tumor formation. In our study, we found that the expression of MIR503HG was significantly reduced in cervical cancer tissues and cell lines. In vitro studies have shown that MIR503HG inhibited cell proliferation and invasion, and enhanced cell apoptosis in cervical cancer through the miR-191/CEBPB axis. MIR503HG regulated the expression of miR-191 via directly binding to miR-191. RESULTS: The expression of MIR503HG had a negative correlation with miR-191 expression in cervical cancer tissues. MiR-191 regulated the expression of CEBPB by directly targeting 3'-UTR of CEBPB mRNA. Overexpression of MIR503HG inhibited cell proliferation, invasion and apoptosis in vitro, and inhibited tumor growth in vivo. CONCLUSIONS: MIR503HG plays a role in suppressing tumors in cervical cancer and is a long-term non-coding RNA.
OBJECTIVE: The long non-coding RNA MIR503 host gene (MIR503HG) plays a role in suppressing or promoting cancer in many types of human malignant tumors. The role of MIR503HG in cervical cancer is still unknown. PATIENTS AND METHODS: The expression level of MIR503HG in cervical cancer tissues and cell lines was accessed using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay. The Cell Counting Kit-8 (CCK-8) assay and flow cytometric analysis were performed to assess cell proliferation and apoptosis in cervical cancer. The nude mouse xenograft experiment was used to examine the ability of MIR503HG in tumor formation. In our study, we found that the expression of MIR503HG was significantly reduced in cervical cancer tissues and cell lines. In vitro studies have shown that MIR503HG inhibited cell proliferation and invasion, and enhanced cell apoptosis in cervical cancer through the miR-191/CEBPB axis. MIR503HG regulated the expression of miR-191 via directly binding to miR-191. RESULTS: The expression of MIR503HG had a negative correlation with miR-191 expression in cervical cancer tissues. MiR-191 regulated the expression of CEBPB by directly targeting 3'-UTR of CEBPB mRNA. Overexpression of MIR503HG inhibited cell proliferation, invasion and apoptosis in vitro, and inhibited tumor growth in vivo. CONCLUSIONS: MIR503HG plays a role in suppressing tumors in cervical cancer and is a long-term non-coding RNA.