Long non-coding RNA fer-1-like family member 4 serves as a tumor suppressor in laryngeal squamous cell carcinoma cells via regulating the AKT/ERK signaling pathway

Abstract

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 RNA s (lncRNA s) 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 (FER 1L4) in the progression of LSCC . The expression levels of FER 1L4 in LSCC cell lines (AMC- HN- 8, Tu 686, M4E and M2E) and a normal cell line (HBE135-E 6E7) were analyzed using reverse transcription-quantitative PCR . The FER 1L4 overexpression plasmid (plasmid-FER 1L4) was subsequently transfected into Tu 686 cells to upregulate the expression levels of FER 1L4. 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-FER 1L4 cells were also treated with insulin-like growth factor 1 (IGF-1) to determine the effect of FER 1L4 on the AKT/ER K signaling pathway, and the effect of the plasmid-FER 1L4 on the expression levels of AKT/ER K signaling pathway-related proteins were analyzed using western blotting. The results of the present study revealed that FER 1L4 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 ER K. Further studies indicated that the aforementioned changes could be reversed by IGF-1, indicating FER 1L4 may regulate the progression of LSCC cells by inhibiting the AKT/ER K signaling pathway. In conclusion, the present study provided a potential novel direction for the treatment of LSCC in the future and suggested that FER 1L4 may be a new target in this field.