LINC00205 facilitates esophageal cancer progression through miR-26a-5p/PTGS2 axis-mediated regulation

The high prevalence of esophageal cancer in China presents a severe challenge to the health of the population and has emerged as a significant public health issue that demands immediate resolution. Through the assessment of the diagnostic efficacy of LINC00205 and the clarification of its regulatory network, this study aims to develop a novel biomarker for esophageal cancer. Individuals diagnosed with esophageal cancer and healthy controls were enrolled ( n = 132/group). Diagnostic efficacy was evaluated using ROC curve analysis. LINC00205 expression was validated by RT-qPCR. Cell biological functions were evaluated using CCK-8, Transwell assays, and flow cytometry. Interactions were determined through RIP and dual-luciferase activity assays. LINC00205 exhibited upregulation in esophageal cancer, demonstrating a significant correlation with patient diagnosis, tumor grading, and N category. miR-26a-5p was recognized as a target of LINC00205 and was downregulated in esophageal cancer. Cellular activities were impeded by the knockdown of LINC00205, and miR-26a-5p inhibitor restored this effect. Moreover, PTGS2, a downstream target of miR-26a-5p, was conspicuously expressed in esophageal cancer. Overexpression of PTGS2 reversed the inhibitory effect of miR-26a-5p mimic on the functions of esophageal cancer cells. LINC00205 may upregulate the expression of PTGS2 through binding to miR-26a-5p, consequently facilitating the malignant progression of esophageal cancer. These findings provide novel insights for the exploration of diagnostic markers in patients.