LINC01980 facilitates esophageal squamous cell carcinoma progression via regulation of miR-190a-5p/MYO5A pathway
Xiaoliang Liang, Zheng Wu, Supeng Shen, Yunfeng Niu, Yanli Guo, Jia Liang, Wei Guo
Abstract
Understanding the role of Long non-coding RNAs (lncRNAs) in tumorigenesis in diverse human malignancies would helpful for targeted therapies, containing esophageal squamous cell carcinoma (ESCC). However, the specific role and molecular mechanisms of LINC01980 in ESCC remain unclarified. In this study, we investigated the expression level, function role, and molecular mechanisms of LINC01980 in esophageal cancer cells and ESCC tissues. The high expression of LINC01980 was detected in ESCC tissues and cells, and predicted poor prognosis. LINC01980 promoted the cell proliferation, migration, invasion ability and epithelial-mesenchymal transition (EMT) progress in ESCC cells. In addition, a negative correlation between LINC01980 and miR-190a-5p or miR-190a-5p and MYO5A was observed in ESCC. We found that miR-190a-5p could directly bind with the mRNA of LINC01980 and MYO5A, and it was detected low expression in ESCC. We further demonstrated that the downregulation of MYO5A caused by overexpressing miR-190a-5p was released via upregulation of LINC01980. Functionally, LINC01980 acted as a competitively endogenous RNA (ceRNA) to impact the expression of MYO5A by sponging miR-190a-5p in ESCC. Therefore, these findings suggest that LINC01980 may act as an oncogenic lncRNA in ESCC and LINC01980/miR-190a-5p/MYO5A pathway contributes to the development of ESCC. • The high expression level of LINC01980 predicted poor prognosis in ESCC. • LINC01980 promoted the tumorigenesis of ESCC by inducing EMT processes. • MiR-190a-5p negatively regulated MYO5A via binding with 3′UTR region. • MiR-190a-5p function as tumor suppressor gene in ESCC. • LINC01980 acted as ceRNA to impact the expression of MYO5A by sponging miR-190a-5p in ESCC.