PMID- 31142627
OWN - NLM
STAT- MEDLINE
DCOM- 20200807
LR  - 20200807
IS  - 1573-4935 (Electronic)
IS  - 0144-8463 (Print)
IS  - 0144-8463 (Linking)
VI  - 39
IP  - 6
DP  - 2019 Jun 28
TI  - Increased expression of lncRNA FTH1P3 predicts a poor prognosis and promotes 
      aggressive phenotypes of laryngeal squamous cell carcinoma.
LID - BSR20181644 [pii]
LID - 10.1042/BSR20181644 [doi]
AB  - 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.
CI  - (c) 2019 The Author(s).
FAU - Yuan, Haozhan
AU  - Yuan H
AD  - Department of Otolaryngology, The First People's Hospital of Xianyang, Xianyang 
      712000, People's Republic of China.
FAU - Jiang, Hong
AU  - Jiang H
AD  - Department of Otolaryngology, The Nuclear Industry 215 Hospital of Shaanxi 
      Province, Xianyang 712000, People's Republic of China.
FAU - Wang, Yanting
AU  - Wang Y
AD  - Department of Otolaryngology, The First People's Hospital of Xianyang, Xianyang 
      712000, People's Republic of China.
FAU - Dong, Yameng
AU  - Dong Y
AUID- ORCID: 0000-0001-5732-5808
AD  - Department of Otolaryngology, The Nuclear Industry 215 Hospital of Shaanxi 
      Province, Xianyang 712000, People's Republic of China dongym92008@tom.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190618
PL  - England
TA  - Biosci Rep
JT  - Bioscience reports
JID - 8102797
RN  - 0 (MicroRNAs)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (long non coding RNA FTH1P3, human)
SB  - IM
MH  - Aged
MH  - Apoptosis/genetics
MH  - Carcinoma, Squamous Cell/*genetics/pathology
MH  - Cell Cycle/genetics
MH  - Cell Line, Tumor
MH  - Cell Movement/genetics
MH  - Cell Proliferation/genetics
MH  - Disease-Free Survival
MH  - Female
MH  - Gene Expression Regulation, Neoplastic/genetics
MH  - Humans
MH  - Laryngeal Neoplasms/*genetics/pathology
MH  - Lymphatic Metastasis
MH  - Male
MH  - MicroRNAs
MH  - Middle Aged
MH  - Phenotype
MH  - *Prognosis
MH  - RNA, Long Noncoding/*genetics
PMC - PMC6580104
OTO - NOTNLM
OT  - FTH1P3
OT  - LSCC
OT  - biomarker
OT  - cell
OT  - prognosis
COIS- The authors declare that there are no competing interests associated with the 
      manuscript.
EDAT- 2019/05/31 06:00
MHDA- 2020/08/08 06:00
PMCR- 2019/06/18
CRDT- 2019/05/31 06:00
PHST- 2018/09/17 00:00 [received]
PHST- 2019/05/09 00:00 [revised]
PHST- 2019/05/22 00:00 [accepted]
PHST- 2019/05/31 06:00 [pubmed]
PHST- 2020/08/08 06:00 [medline]
PHST- 2019/05/31 06:00 [entrez]
PHST- 2019/06/18 00:00 [pmc-release]
AID - BSR20181644 [pii]
AID - 10.1042/BSR20181644 [doi]
PST - epublish
SO  - Biosci Rep. 2019 Jun 18;39(6):BSR20181644. doi: 10.1042/BSR20181644. Print 2019 
      Jun 28.