High expression of interleukin‑enhancer binding factor 3 predicts poor prognosis in patients with lung adenocarcinoma

Abstract

Interleukin-enhancer binding factor 3 (ILF3) is a double-stranded RNA-binding protein that has been reported to contribute to the occurrence and progression of various malignant tumors. The aim of the present study was to evaluate the prognostic value of ILF3 and to apply this knowledge to avoid excessive medical treatment in patients with lung adenocarcinoma (LUAD). ILF3 expression in a discovery set consisting of tumor and peri-tumor tissue microarrays was analyzed using immunohistochemical methods. The mRNA level of ILF3 was subsequently analyzed in a validation set downloaded from The Cancer Genome Atlas. The Kaplan-Meier method, univariate and multivariate Cox analyses, decision curve analysis and nomogram models were used to evaluate the prognostic value of ILF3. ILF3 expression was upregulated in tumor tissues compared with peri-tumor tissues and was negatively associated with the overall survival time of patients with LUAD in the discovery and validation sets. Moreover, ILF3 expression was used for risk stratifica-tion in patients with tumor-node-metastasis stages II-IV and poor-to-moderate tumor differentiation. ILF3 expression was identified as an independent predictor of adverse prognosis for patients with LUAD in the discovery and validation sets. Finally, nomogram models for the 3-and 5 year survival time of patients with LUAD revealed that ILF3 expression may be used to improve the predictive accuracy of the prognosis and to avoid excessive medical treatment for certain patients with the disease. Overall, the data obtained in the current study revealed that high ILF3 expression was associated with poor prognosis, and demonstrated that ILF3, as a potential independent risk factor, may improve the hierarchical postoperative management of patients with LUAD.

DNA and RNA Binding Proteins: From Motifs to Roles in Cancer

“…Interleukin enhancer-binding factor 3 (ILF3) and ILF2 (also named NF45) were originally discovered as positive regulators of IL2 transcription as part of the NFAT-AP1-NF-kB enhanceosome in activated T-cells and have roles in cancer [ 157 , 158 , 159 ], autoimmune and inflammatory conditions [ 160 , 161 ], and psychiatric disorders [ 162 ]. ILF3 and ILF2 are involved in almost all steps of RNA metabolism, including transcription, post transcription, translation, pri-miRNA, lncRNA, circular RNA processing, and RNA editing [ 163 , 164 ].…”

Ox-LDL-mediated ILF3 overexpression in gastric cancer progression by activating the PI3K/AKT/mTOR signaling pathway

“…For example, ILF3 facilitated the occurrence of colorectal cancer by regulating the mRNA stability of serine–glycine–one-carbon (SGOC) SGOC genes [ 27 ]. ILF3 overexpression was associated with poor clinical outcome for patients with lung cancer, and ILF3 can also be employed to guide the hierarchical postoperative management of patients with lung cancer [ 28 ]. ILF3 might serve as an important promoter in hepatocellular carcinoma proliferation and migration, and could be a potential therapeutic target in hepatocellular carcinoma [ 29 ].…”