Downregulation of Long Noncoding RNA in Non-Homologous End Joining Pathway 1 Inhibits the Progression of Esophageal Squamous Cell Carcinoma

Background: Long noncoding RNA (lncRNA) in non-homologous end joining pathway 1 (LINP1) contributes to tumorigenesis in various cancers. However, little is known about the role of LINP1 in esophageal squamous cell carcinoma (ESCC). Methods: LINP1 was selected as the target lncRNA by bioinformatics analysis. The correlation between LINP1 expression and prognosis was analyzed in 122 ESCC patients. LINP1 status was evaluated by fluorescence in situ hybridization (FISH) in normal esophageal tissue, ESCC, and EC9706 cells. LINP1 was silenced by short hairpin (sh)RNA transfection in EC9706 cells, and the biological function and molecular mechanism were evaluated. In vitro results were verified by xenograft tumor assays. Findings: Bioinformatics analysis showed that LINP1 was the most significantly differentially expressed lncRNA. High LINP1 expression in ESCC patients was significantly associated with poor prognosis (P = 0.034). FISH assay showed that LINP1 was highly expressed in ESCC tissues and EC9706 cells. LINP1 knockdown decreased the proliferative and migratory abilities of ESCC cells, and promoted cell apoptosis and cell cycle arrest at the G2/GM phase. Epithelial-mesenchymal transition related proteins such as N-cadherin, vimentin, and snail were downregulated while E-cadherin was up-regulated significantly in shRNA-LINP1 cells. In the xenograft model, knockdown of LINP1 suppressed ESCC tumorigenesis in vivo. Interpretation: LINP1 knockdown inhibited the carcinogenic progression of ESCC. LINP1 was identified as a potential prognostic biomarker and therapeutic target in ESCC. Funding Statement: This study was supported by Shanghai Sailing Program (No. 17YF1402400). Declaration of Interests: The authors state: None. Ethics Approval Statement: The study was approved by the hospital ethics committee and all patients signed an informed consent form.