Uterus corpus endometrial cancer (UCEC) is associated with a high mortality rate. In this study, we examined the impact of long intergenic non-protein coding RNA 01234 (LINC01234) in the diagnosis and survival of UCEC using an open high-throughput sequencing database. The association between LINC01234 expression and UCEC clinical features was determined using the Wilcoxon rank sum test, logistic regression and Cox regression. To assess the classification effectiveness of LINC01234 in UCEC, the area under the receiver operating characteristic (ROC) curve (AUC) was performed. Then, Kaplan-Meier analysis was performed to determine the prognostic significance of LINC01234 in UCEC. The underlying regulatory mechanisms of LIN01234 were assessed using the Gene set enrichment analysis (GSEA), and the influence on immune infiltration cells was tested by the Spearman correlation method. Datebases showed LINC01234 was up-regulated in UCEC and associated with poor clinicopathologic characteristics. What’s more quantitative real time polymerase chain reaction (qRT-PCR) analyse of clinical tissue specimens, LINC01234 was actually high expression in UCEC. The results showed an AUC of 0.726, indicating that LINC01234 had a significant diagnostic value. Further, Kaplan-Meier analysis showed that high LINC01234 expression was associated with poorer progress free interval (PFI) (hazard ratio (HR): 1.68, 95% confidence interval (CI): 1.18–2.39, p = 0.004), disease-specific survival (DSS) (HR: 2.17, 95% CI: 1.29–3.67, p = 0.004), overall survival (OS) (HR: 1.81, 95% CI: 1.19–2.75, p = 0.005). Cox regression analysis showed LINC01234 expression was an independent factor for DSS. Pathway enrichment and immune infiltration analysis showed the most likely mechanisms that LINC01234 promoted tumor progression. LINC01234 demonstrated diagnostic and prognostic potential in UCEC and was shown to exert its effects via various mechanisms, including cell proliferation, spermatogenesis, angiogenesis and immune response in the tumor microenvironment, to promote tumor progression; thus, indicating that it could be a target for treating UCEC.