Increased expression of lncRNA FTH1P3 predicts a poor prognosis and promotes aggressive phenotypes of laryngeal squamous cell carcinoma.
Aged
Apoptosis
/ genetics
Carcinoma, Squamous Cell
/ genetics
Cell Cycle
/ genetics
Cell Line, Tumor
Cell Movement
/ genetics
Cell Proliferation
/ genetics
Disease-Free Survival
Female
Gene Expression Regulation, Neoplastic
/ genetics
Humans
Laryngeal Neoplasms
/ genetics
Lymphatic Metastasis
Male
MicroRNAs
Middle Aged
Phenotype
Prognosis
RNA, Long Noncoding
/ genetics
FTH1P3
LSCC
biomarker
cell
prognosis
Journal
Bioscience reports
ISSN: 1573-4935
Titre abrégé: Biosci Rep
Pays: England
ID NLM: 8102797
Informations de publication
Date de publication:
28 06 2019
28 06 2019
Historique:
received:
17
09
2018
revised:
09
05
2019
accepted:
22
05
2019
pubmed:
31
5
2019
medline:
8
8
2020
entrez:
31
5
2019
Statut:
epublish
Résumé
Laryngeal squamous cell cancer (LSCC) is a highly aggressive malignancy in the head and neck region. Recent studies have shown that long noncoding RNAs (lncRNAs) are novel transcripts that play an important role in the progression of LSCC. However, the overall pathophysiological regulation of lncRNAs to LSCC is largely unknown. The present study aimed to determine the clinical significances of lncRNA ferritin heavy chain 1 pseudogene 3 (FTH1P3) and to identify its potential roles in LSCC. Quantitative real-time PCR (qRT-PCR) showed that FTH1P3 expression was significantly up-regulated in LSCC tissues than that in non-neoplastic tissues. High FTH1P3 expression was positively correlated with the poor differentiation, high T classification, positive lymph node metastasis, and advanced clinical stage. Overall survival analysis showed that high levels of FTH1P3 predicted a poor prognosis in LSCC patients. Moreover, elevated expression of FTH1P3 was found to increase LSCC cell proliferation, migration and invasion, and to inhibit cell apoptosis, Conversely, knockdown of FTH1P3 suppressed LSCC cell proliferation, migration and invasion, and induced cell apoptosis. In addition, overexpression of FTH1P3 resulted in an increase in cells in S phase and a decrease in cells in G0/G1 phase, whereas inhibition of FTH1P3 did the opposite effects. Taken together, these results suggested that increased expression of FTH1P3 predicts a poor prognosis and promotes aggressive phenotypes of LSCC by regulating cell proliferation, migration, invasion, apoptosis, and cell cycle, indicating FTH1P3 may serve as a promising therapeutic biomarker for the treatment of LSCC.
Identifiants
pubmed: 31142627
pii: BSR20181644
doi: 10.1042/BSR20181644
pmc: PMC6580104
pii:
doi:
Substances chimiques
MicroRNAs
0
RNA, Long Noncoding
0
long non coding RNA FTH1P3, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© 2019 The Author(s).
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