Elf1, also known as E74-like factor 1, is a transcription factor belonging to the Ets family. It plays diverse roles in multiple biological processes. In transcription, it has been associated with transcription-coupled repair pathways [4,8]. In the context of immunity, it is involved in macrophage development [5]. It also has implications in cell proliferation, migration, and autophagy regulation, thus being linked to various disease-related pathways [2,3,6]. Genetic models such as zebrafish are valuable for studying its functions [5].

In systemic lupus erythematosus (SLE) patients, ELF1 gene expression is significantly downregulated in CD4+ T cells compared to healthy controls. Its expression is also decreased in certain SLE subgroups, and ROC curve analysis indicates its diagnostic potential for SLE, as well as its value in assessing disease activity and renal involvement [1]. In early pregnancy loss (EPL), ELF1 is lowly expressed in placental villous tissues. Overexpression of ELF1 promotes proliferation and migration of trophoblast cells, suggesting its role in EPL [2]. In glioma, high expression of ELF1 may be related to the malignant behavior of the tumor, as silencing ELF1 inhibits glioma cell growth and migration with ATF5 involvement [3]. In lung cancer cells, ELF1 suppresses autophagy to reduce cisplatin resistance via the miR-152-3p/NCAM1/ERK axis [6]. In gastric cancer, ELF1 is overexpressed and combined with MMP9, it can serve as a predictor of malignant biological behavior and a prognostic indicator, being associated with the tumor microenvironment [7].

In conclusion, Elf1 has essential functions in transcription-coupled repair, macrophage development, and processes related to cell proliferation, migration, and autophagy. Its study through model-based research has revealed its significance in diseases like SLE, EPL, glioma, lung cancer, and gastric cancer. These findings provide insights into disease mechanisms and potential therapeutic targets.