Abstract
Background and objectives: Due to its lack of early symptoms, cholangiocarcinoma (CCA) is frequently diagnosed at advanced stages, contributing to its dismal prognosis. Therefore, it is necessary to find new, efficient therapeutic methods for the disease. This study excavated the role of LINC00519 in CCA progression, aiming to provide useful insights into CCA treatment. Materials and methods: This study collected tumor and normal paracancer tissues from CCA patients (n = 202) to explore the prognostic significance of LINC00519 in CCA. CCA cell lines CCLP1 and QBC939 were employed for detecting the role of LINC00519 on CCA tumor development. The qRT-PCR was used to measure the expression of biomolecules. Cell Counting Kit-8 (CCK-8) and transwell assay were used to estimate CCA cell proliferation, migration and invasion. Binding sites between biomolecules were verified using a dual luciferase reporter assay. Results: LINC00519 was upregulated in CCA. The upregulation of LINC00519 was associated with poor prognosis and serverity in CCA patients. LINC00519 facilitated CCA progression by promoting CCA cell proliferation rate, as well as cell migration and invasion ability. The approach for LINC00519 altering CCA cell activities was to inhibit miR-876-3p, and miR-876-3p could further negatively regulate GATA1. Conclusion: LINC00519 upregulation may serve as a potential indicator of CCA aggravation. LINC00519 promoted CCA development by targeting miR-876-3p to affect cancer cell activities. GATA1, a potential target of miR-876-3p, suggests the potential underlying molecular pathway. Targeting LINC00519 could be an efficient way to manage CCA.