PMID- 29280495
OWN - NLM
STAT- MEDLINE
DCOM- 20181004
LR  - 20181004
IS  - 1531-4995 (Electronic)
IS  - 0023-852X (Linking)
VI  - 128
IP  - 4
DP  - 2018 Apr
TI  - TSR2 Induces laryngeal cancer cell apoptosis through inhibiting NF-kappaB signaling 
      pathway.
PG  - E130-E134
LID - 10.1002/lary.27035 [doi]
AB  - OBJECTIVES/HYPOTHESIS: Human laryngeal squamous cell carcinoma (LSCC) is a 
      malignancy that was discovered originally in the epithelial tissue of laryngeal 
      mucosa. However, the underlying molecular mechanism is still not clear. In this 
      study, we aimed to investigate the potential molecular mechanisms of TSR2 in the 
      LSCC cell apoptosis. STUDY DESIGN: The expression of TSR2 was first analyzed in 
      LSCC tissues. Then functional effects of TSR2 on Hep-2 and AMC-HN-8 cell lines 
      were performed by overexpression pcDNA3.1-TSR2. METHODS: We investigated the 
      expression level of TSR2 in LSCC tissues and cells by performing quantitative 
      real-time polymerase chain reaction (qRT-PCR). The pcDNA3.1-TSR2 was constructed 
      to explore the effect of overexpressing TSR2 in Hep-2 cells and AMC-HN-8 cells. 
      We further investigated the effect of overexpressing TSR2 on cell 
      apoptosis-related protein and nuclear factor kappa-light-chain-enhancer of 
      activated B cells (NF-kappaB) p65 nuclear translocation through Western blot and 
      terminal dUTP nick end-labeling assays. RESULTS: We found that TSR2 was 
      downregulated in LSSC tissues and cells compared with the controls, and the 
      overexpression of TSR2 in Hep-2 and AMC-HN-8 cells could promote cell apoptosis 
      and related apoptosis proteins. The Western blot/qRT-PCR data further indicated 
      that overexpression of TSR2 in Hep-2 and AMC-HN-8 cells could lead to a block of 
      NF-kappaB signaling pathway via decreasing nuclear NF-kappaB p65 and increasing cytoplasm 
      NF-kappaB p65. Moreover, overexpression of TSR2 significantly inhibited the 
      phosphorylation of IkappaBalpha and IKKalpha/beta. CONCLUSIONS: The results indicated that 
      TSR2-induced apoptosis was mediated by inhibiting the NF-kappaB signaling pathway, 
      which may provide an effective target in gene therapy for LSCC. LEVEL OF 
      EVIDENCE: NA. Laryngoscope, 128:E130-E134, 2018.
CI  - (c) 2017 The American Laryngological, Rhinological and Otological Society, Inc.
FAU - He, Hong-Jiang
AU  - He HJ
AUID- ORCID: 0000-0002-8354-0365
AD  - Department of Head and Neck Surgery, Affiliated Tumor Hospital of Harbin Medical 
      University, Harbin, China.
FAU - Bing, Han
AU  - Bing H
AD  - Department of Ophthalmology, Hospital of Heilongjiang Province, Harbin, China.
FAU - Liu, Guijun
AU  - Liu G
AD  - Heilongjiang University of Chinese Medicine, Heilongjiang Province, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20171227
PL  - United States
TA  - Laryngoscope
JT  - The Laryngoscope
JID - 8607378
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (TSR2 protein, human)
RN  - 0 (Transcription Factor RelA)
SB  - IM
MH  - Apoptosis/*physiology
MH  - Apoptosis Regulatory Proteins/*physiology
MH  - Blotting, Western
MH  - Carcinoma, Squamous Cell/*metabolism
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - Down-Regulation
MH  - Humans
MH  - Laryngeal Neoplasms/*metabolism
MH  - Larynx/metabolism
MH  - NF-kappa B/*metabolism
MH  - Signal Transduction/physiology
MH  - Transcription Factor RelA/metabolism
OTO - NOTNLM
OT  - Human laryngeal squamous cell carcinoma
OT  - NF-kappaB
OT  - TSR2
OT  - cell apoptosis
EDAT- 2017/12/28 06:00
MHDA- 2018/10/05 06:00
CRDT- 2017/12/28 06:00
PHST- 2017/05/23 00:00 [received]
PHST- 2017/10/24 00:00 [revised]
PHST- 2017/11/03 00:00 [accepted]
PHST- 2017/12/28 06:00 [pubmed]
PHST- 2018/10/05 06:00 [medline]
PHST- 2017/12/28 06:00 [entrez]
AID - 10.1002/lary.27035 [doi]
PST - ppublish
SO  - Laryngoscope. 2018 Apr;128(4):E130-E134. doi: 10.1002/lary.27035. Epub 2017 Dec 
      27.