PMID- 33174027
OWN - NLM
STAT- MEDLINE
DCOM- 20210510
LR  - 20210510
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 22
IP  - 6
DP  - 2020 Dec
TI  - 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.
PG  - 5304-5312
LID - 10.3892/mmr.2020.11598 [doi]
AB  - 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.
FAU - Jiao, Lulu
AU  - Jiao L
AD  - Department of Otorhinolaryngology, Dongzhimen Hospital, Beijing University of 
      Chinese Medicine, Beijing 100700, P.R. China.
FAU - Liu, Siming
AU  - Liu S
AD  - Department of Otorhinolaryngology, Dongzhimen Hospital, Beijing University of 
      Chinese Medicine, Beijing 100700, P.R. China.
FAU - Liu, Lili
AU  - Liu L
AD  - Department of Otorhinolaryngology, Dongzhimen Hospital, Beijing University of 
      Chinese Medicine, Beijing 100700, P.R. China.
FAU - Hao, Pengpeng
AU  - Hao P
AD  - Department of Otorhinolaryngology, Dongzhimen Hospital, Beijing University of 
      Chinese Medicine, Beijing 100700, P.R. China.
FAU - Gong, Zheng
AU  - Gong Z
AD  - Department of Otorhinolaryngology, Dongzhimen Hospital, Beijing University of 
      Chinese Medicine, Beijing 100700, P.R. China.
FAU - Yan, Zhanfeng
AU  - Yan Z
AD  - Department of Otorhinolaryngology, Dongzhimen Hospital, Beijing University of 
      Chinese Medicine, Beijing 100700, P.R. China.
FAU - Xiang, Yinzhou
AU  - Xiang Y
AD  - Department of Otorhinolaryngology, Taizhou First People's Hospital, Taizhou, 
      Zhejiang 318020, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20201014
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (long non-coding RNA FER1L4, human)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Apoptosis/genetics
MH  - Carcinoma, Squamous Cell/pathology
MH  - Cell Line, Tumor
MH  - Cell Movement/genetics
MH  - Cell Proliferation/genetics
MH  - Cell Survival
MH  - Gene Expression Regulation, Neoplastic/genetics
MH  - Genes, Tumor Suppressor/physiology
MH  - Head and Neck Neoplasms/genetics
MH  - Humans
MH  - Laryngeal Neoplasms/genetics
MH  - MAP Kinase Signaling System/genetics
MH  - MicroRNAs/genetics
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - RNA, Long Noncoding/*genetics/metabolism
MH  - Signal Transduction/genetics
MH  - Squamous Cell Carcinoma of Head and Neck/*genetics
PMC - PMC7647000
EDAT- 2020/11/12 06:00
MHDA- 2021/05/11 06:00
PMCR- 2020/10/14
CRDT- 2020/11/11 06:00
PHST- 2020/06/10 00:00 [received]
PHST- 2020/08/26 00:00 [accepted]
PHST- 2020/11/12 06:00 [pubmed]
PHST- 2021/05/11 06:00 [medline]
PHST- 2020/11/11 06:00 [entrez]
PHST- 2020/10/14 00:00 [pmc-release]
AID - mmr-22-06-5304 [pii]
AID - 10.3892/mmr.2020.11598 [doi]
PST - ppublish
SO  - Mol Med Rep. 2020 Dec;22(6):5304-5312. doi: 10.3892/mmr.2020.11598. Epub 2020 Oct 
      14.