LINC01410/miR-23c/CHD7 functions as a ceRNA network to affect the prognosis of patients with endometrial cancer and strengthen the malignant properties of endometrial cancer cells.

In previous studies, long non-coding RNA LINC01410 (LINC01410) has been found to promote cells proliferation and invasion in colon and gastric cancers. However, the function of LINC01410 in endometrial cancer (EC) is still elusive. The expression patterns of LINC01410/miR-23c/Chromodomain Helicase DNA-Binding Protein 7 (CHD7) in EC tissues and the prognosis of patients with different expression of LINC01410/miR-23c/CHD7 were determined by consulting TCGA database. EC patients with complete clinical data were applied for clinicopathological correlation analysis. The biological characteristics of EC cells were analyzed with the support of CCK-8 and transwell assays. CHD7 expression was assessed by qRT-PCR and western blot assays. Targeted associations between LINC01410 and miR-23c, as well as miR-23c and CHD7 were speculated by prediction website and verified by dual-luciferase assay. Rescue assays were performed to explore the interrelation among LINC01410, miR-23c and CHD7. Our data illustrated that LINC01410 high expression was presented in EC tissues and was positively related to the poor prognosis of patients in EC, as well as the malignant behaviors of EC cells. Through bioinformatics analysis, we surmised that LINC01410/miR-23c/CHD7 may play a role through the formation of competing endogenous RNA (ceRNA) mechanism. CHD7 expression was positively regulated by LINC01410, and inversely controlled by miR-23c. Furthermore, the promoting effects of miR-23c inhibitor or CHD7 upregulation on EC cell growth and aggressiveness were attenuated by LINC01410 silencing. Our results indicated that high expression of LINC01410 promoted EC cell progression through modulating miR-23c/CHD7 axis, providing a new direction for revealing the molecular mechanism of EC.

KEYWORDS: {{ getKeywords(articleDetailText.words) }}