DSCAM-AS1 promotes cervical carcinoma cell proliferation and invasion via sponging miR-338-3p

• DOI: 10.1007/s11356-022-19962-w
• Publication Date: 2022-04-04T20:02:31Z
• Authors: Chunmei Li; Xiaoqiong Li; Yi Zhang; Liangzhi Wu; Jingjun He; Nan Jiang; Hui Zhao; Wenwen Liu
• Keywords: Gene Expression Regulation, Neoplastic; 0301 basic medicine; MicroRNAs; 03 medical and health sciences; Cell Line, Tumor; Carcinoma; Humans; Uterine Cervical Neoplasms; Female; RNA, Long Noncoding; Cell Proliferation; 3. Good health

Deregulated lncRNA DSCAM-AS1 expression was found in several tumors. However, mechanism and functional role of DSCAM-AS1 in cervical carcinoma remain unknown. DSCAM-AS1 was detected in cervical carcinoma specimens and cells by RT-qPCR. CCK-8, Matrigel transwell, and flow cytometry were conducted to determine cell functions. In this research, we firstly we explored DSCAM-AS1 expression in cervical carcinoma cells and specimens. We revealed that DSCAM-AS1 was upregulated in cervical carcinoma lines (C4-1, Caski, Hela, and Siha) compared to GH329 cells. DSCAM-AS1 was upregulated in cervical carcinoma specimens compared to control no-tumor specimens. Overexpression of DSCAM-AS1 induced cervical carcinoma cell growth and cycle. Moreover, our data revealed that miR-338-3p expression was downregulated in cervical carcinoma cells and specimens. There was a negative correlation between miR-338-3p expression and DSCAM-AS1 expression in cervical carcinoma specimens. Elevated expression of miR-338-3p decreased cervical carcinoma cell growth and cycle and invasion. Furthermore, luciferase reporter analysis revealed that miR-338-3p overexpression suppressed luciferase activity of WT-DSCAM-AS1 vector but not the mut-DSCAM-AS1. Ectopic expression of DSCAM-AS1 decreased miR-338-3p expression in the Siha cell. Overexpression of DSCAM-AS1 promoted cervical carcinoma cell growth and cycle via regulating miR-338-3p. These results suggested that DSCAM-AS1 functions as one oncogene through sponging miR-338-3p in cervical carcinoma.