LINC00942 Accelerates Esophageal Cancer Progression by Raising PRKDC Through Interaction With PTBP1

ABSTRACT Aberrantly expressed LINC00942 is participated in the progression of several cancers. However, the function of LINC00942 in esophageal cancer (ESCA) is unclear. The objective of this study was to explore the effect of LINC00942 on ESCA and its possible molecular mechanisms. First, differentially expressed lncRNAs in ESCA were analyzed using GSE192662 microarray. catRAPID omics v2.1 was applied to predict the proteins that might interact with LINC00942. SDS‐PAGE silver staining assay, RNA pull down, and RIP assay were utilized to validate proteins interacting with LINC00942. Then, RNA seq was applied to detect the downstream targets of PTBP1, and KEGG enrichment analysis was used to analyze the genes involved in proliferation and migration‐related signaling pathways. In addition, CCK‐8, EdU and transwell were used to detect the impact of LINC00942 on ESCA cell function. Bioinformatics revealed that LINC00942 was significantly overexpressed in ESCA. Patients in low‐expression of LINC00942 had an obviously better prognosis. After LINC00942 knockdown, the proliferation and migration of TE‐1 and OE19 were dramatically reduced. Subsequently, PTBP1 was found to interact with LINC00942, and PRKDC was a downstream target of PTBP1. Functional analysis showed that TE‐1 and OE19 cell proliferation and migration were markedly elevated after LINC00942 overexpression, and knockdown of PRKDC significantly reversed this effect. Mechanistically, LINC00942 promoted PRKDC expression by interacting with PTBP1. In summary, LINC00942 facilitated the proliferation and migration of ESCA cells via binding to PTBP1 to promote PRKDC expression.