laryngeal squamous cell carcinoma (lScc) is a common type of malignant tumor of the head and neck. an increasing number of studies have illustrated that long non-coding rnas (lncrnas) serve an important role in the occurrence and development of lScc. Therefore, the present study aimed to investigate the expression changes and mechanism of lncrna fer-1-like family member 4 (Fer1l4) in the progression of lScc. The expression levels of Fer1l4 in lScc cell lines (aMc-Hn-8, Tu 686, M4e and M2e) and a normal cell line (HBe135-e6e7) were analyzed using reverse transcription-quantitative Pcr. The Fer1l4 overexpression plasmid (plasmid-Fer1l4) was subsequently transfected into Tu 686 cells to upregulate the expression levels of Fer1l4. cell viability was detected using a cell counting Kit-8 assay, cell proliferation was analyzed using a colony formation assay, apoptosis was examined by flow cytometry, and cell migration and invasion were determined using wound healing and Transwell assays, respectively. in addition, the plasmid-Fer1l4 cells were also treated with insulin-like growth factor 1 (iGF-1) to determine the effect of Fer1l4 on the aKT/erK signaling pathway, and the effect of the plasmid-Fer1l4 on the expression levels of aKT/erK signaling pathway-related proteins were analyzed using western blotting. The results of the present study revealed that Fer1l4 expression levels were downregulated in aMc-Hn-8 and Tu 686 cells. Notably, FER1L overexpression significantly reduced the cell viability, proliferation, migration and invasion of lScc cells, while promoting apoptosis. Meanwhile, the plasmid-FER1L4 also significantly suppressed the phosphorylation levels of aKT and erK. Further studies indicated that the aforementioned changes could be reversed by iGF-1, indicating Fer1l4 may regulate the progression of lScc cells by inhibiting the aKT/erK signaling pathway. in conclusion, the present study provided a potential novel direction for the treatment of lScc in the future and suggested that Fer1l4 may be a new target in this field.