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.