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 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.

Editorial: “Non-Coding RNAs in Head and Neck Squamous Cell Carcinoma”

“…Besides, some of lncRNAs functionally act as tumor suppressors, e.g., lincRNA–p21 ( 27 ) or LINC02487( Feng et al. ), long non–coding RNA Fer–1–like protein 4 (FER1L4) ( 28 ), and growth arrest specific 5 (GAS5) ( 29 ), but others play an oncogenic role, e.g., ring finger and CCCH–type domains 2 (RC3H2) ( 30 ), FOXD2 adjacent opposite strand RNA 1(FOXD2–AS1) ( 31 ), KTN1 antisense RNA 1(KTN1–AS1) ( 32 ), LINC00460 ( 33 ), H19 imprinted maternally expressed transcript (H19) ( 34 ), small nucleolar RNA host gene 6 (SNHG6) ( 35 ), urothelial cancer associated 1 (UCA1) ( 36 ), or ZNFX1 antisense RNA 1 (ZFAS1) ( 37 ), and can be used as therapeutic targets in the future. More and more evidences show that multiple lncRNAs–based signatures could be diagnostic and prognostic predictors of HNSCC patients by mathematical modeling.…”

LncRNA CCAT1 facilitates the proliferation, invasion and migration of human laryngeal squamous cell carcinoma cells via the miR-218-5p/BMI1

“…LncRNAs can radically manipulate several cellular processes in different diseases and cancers ( Zhang & Tang, 2018 ). Recent investigations have elicited the regulatory effects of several lncRNAs including IUR, WTAPP1, and FER1L4 on cell migration, proliferation, and invasion in LSCC ( Jiao et al, 2020 ; Shi et al, 2020 ; Wei et al, 2020 ). Among the numerous lncRNAs, lncRNA colon cancer-associated transcript-1 (CCAT1) has attracted our attention.…”