Knockdown of Long Noncoding RNA LINC00240 Inhibits Esophageal Cancer Progression by Regulating miR-26a-5p

Abstract

Background. Esophageal cancer is the most prevalent digestive system tumor. Due to a lack of characteristic symptoms and early diagnosis, a confirmed esophageal cancer is typically detected at a progressively harmful stage. Therefore, it is critical to investigate the molecular mechanisms governing the formation and progression of esophageal cancer in order to identify new treatment targets for esophageal cancer early detection. Methods. We first screened the differentially expressed gene LINC00240 in the TCGA database. Multivariate analysis and Cox regression were performed, and a nomogram was constructed for internal validation. The correlation between LINC00240 and immune cells was analyzed using the TIMER database. The possible mechanism of action was explored through GSEA enrichment analysis. Then, in 43 esophageal cancer tissues, paracancour tissues, and cell lines, the LINC00240 expression was found. Transwell assays, CCK-8, and clone formation assays were utilized to assess the impact of LINC00240 on the metastasis of esophageal cancer cells. The binding activity of LINC00240 to downstream miRNAs was assessed using the luciferase reporter gene. Results. TCGA database showed that LINC00240 expression was increased in cancer tissues compared to adjacent tissues. The C-index of the nomogram is 0.712 (0.666–0.758), and the prediction model has good accuracy. According to the TIMER database, the LINC00240 expression is linked to immune infiltration and may be crucial in encouraging the immune escape of tumor cells. Gene enrichment analysis depicts that LINC00240 could influence the biological events of esophageal cancer by taking part in pathways such as affecting the cell cycle. LINC00240 expression was substantially greater in the plasma of esophageal cancer patients (3.94 ± 1.55) than in the normal control group (2.13 ± 0.89). Plasma expression of LINC00240 was linked to the degree of differentiation ( $P=0.0345$ ) and TNM stage ( $P=0.0409$ ). Knocked down LINC00240 inhibited esophageal cancer cells proliferation, lone formation, and invasion. LINC00240 might bind itself to miR-26a-5p and influence its expression. MiR-26a-5p inhibitor can dramatically limit the ability of LINC00240 knockdown on plate colony formation and relocation of esophageal cancerous cells was demonstrated in colony formation and migration experiments. Conclusion. LINC00240 expression is elevated in esophageal cancerous tissues, and knocking down LINC00240 decreases esophageal cancer cell proliferation, clone formation, invasion, and migration via miR-26a-5p. As a result, LINC00240 could be a novel target for esophageal cancer patients' early diagnosis and treatment.