Eif3l, the eukaryotic translation initiation factor 3, subunit L, is one subunit of the eIF3 complex. As an initiation factor, it plays a key role in the translation of mRNAs encoding growth-promoting proteins by enhancing translation rates, thus controlling cell proliferation. It is also involved in processes like Flavivirus replication through interaction with the viral non-structural 5 protein [2,4].

Mutations in eif-3.L gene in Caenorhabditis elegans result in a 40% extension in lifespan and enhanced resistance to endoplasmic reticulum (ER) stress. These mutants show normal growth and development and wild-type levels of bulk protein synthesis. Lifespan extension is suppressed by a mutation in the Forkhead family transcription factor DAF-16, and enhanced ER stress resistance is independent of IRE-1-XBP-1, ATF-6, PEK-1, and DAF-16 [3]. In human prostate LNCaP cells, androgen treatment significantly increases the palmitoylation level of eIF3L, and the regulation of its palmitoylation may provide new directions for prostate cancer therapy, with increased eIF3L levels potentially serving as an early-stage prostate cancer biomarker [1].

In conclusion, Eif3l is crucial for cell proliferation through its role in mRNA translation. Studies in Caenorhabditis elegans and human prostate cells have revealed its significance in lifespan regulation, stress response, and cancer-related processes. These findings from model-based research contribute to understanding disease mechanisms, especially in the context of prostate cancer and aging-related ER stress responses.