Ontology highlight
ABSTRACT: Background
DLEU2 is a long noncoding RNA considered important in the progression of many cancers. However, correlations between DLEU2 and kidney renal clear cell carcinoma (KIRC) and liver hepatocellular carcinoma (LIHC) have rarely been reported. Methods
We first analysed the expression of DLEU2 across cancers and the correlation between DLEU2 and the clinical features of KIRC and LIHC by using the “ggplot2” package in R and searched the Oncomine database and Timer website platform. We verified the expression of DLEU2 in the GEO dataset (GSE105261 and GSE45267). Receiver operating characteristic (ROC) curves were drawn using the “pROC” and “ggplot2” packages in R, and we constructed a DLEU2-based prognostic nomogram for KIRC and LIHC by using the “survival” and “rms” packages in R. Then, we analysed the correlation between DLEU2 expression and prognosis in R as well as the correlation between DLEU2 and immune cell infiltration in the TIMER database. Finally, we explored the causes of DLEU2 upregulation in the UCSC Xena and UALCAN databases. Results
We found that DLEU2 was upregulated in many cancers, including KIRC and LIHC. Expression of DLEU2 is associated with tumour stage, grade, lymphatic metastasis, and distant metastasis in KIRC as well as alpha-fetoprotein (AFP), tumour stage, grade, lymphatic metastasis, and distant metastasis in LIHC. DLEU2 is an adverse factor for the prognosis of KIRC and LIHC. In addition, DLEU2 has moderate accuracy in diagnosing KIRC and LIHC and predicting their prognosis. Moreover, we found that expression of DLEU2 correlated positively with immune cell infiltration in KIRC and LIHC, and upregulation of DLEU2 in KIRC and LIHC suggests a poor prognosis based on immune cells analysis. Genetic and epigenetic analyses of DLEU2 indicate that copy number variations (CNVs) and methylation contribute to the upregulation of DLEU2. Conclusion
The long noncoding RNA DLEU2 has the potential to predict the prognosis and immune infiltration of KIRC and LIHC.
SUBMITTER: Fu S
PROVIDER: S-EPMC8593347 | biostudies-literature |
REPOSITORIES: biostudies-literature