PMID- 23977169
OWN - NLM
STAT- MEDLINE
DCOM- 20140408
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 8
IP  - 8
DP  - 2013
TI  - The function and significance of SELENBP1 downregulation in human bronchial 
      epithelial carcinogenic process.
PG  - e71865
LID - 10.1371/journal.pone.0071865 [doi]
LID - e71865
AB  - BACKGROUND: Our quantitative proteomic study showed that selenium-binding protein 
      1 (SELENBP1) was progressively decreased in human bronchial epithelial 
      carcinogenic process. However, there is little information on expression and 
      function of SELENBP1 during human lung squamous cell cancer (LSCC) 
      carcinogenesis. METHODS: iTRAQ-tagging combined with 2D LC-MS/MS analysis was 
      used to identify differentially expressed proteins in the human bronchial 
      epithelial carcinogenic process. SELENBP1, member of selenoproteins family and 
      progressively downregulated in this process, was selected to further study. Both 
      Western blotting and immunohistochemistry were performed to detect SELENBP1 
      expression in independent sets of tissues of bronchial epithelial carcinogenesis, 
      and ability of SELENBP1 for discriminating NBE (normal bronchial epithelium) from 
      preneoplastic lesions from invasive LSCC was evaluated. The effects of SELENBP1 
      downregulation on the susceptibility of benzo(a)pyrene (B[a]P)-induced human 
      bronchial epithelial cell transformation were determined. RESULTS: 102 
      differentially expressed proteins were identified by quantitative proteomics, and 
      SELENBP1 was found and confirmed being progressively decreased in the human 
      bronchial epithelial carcinogenic process. The sensitivity and specificity of 
      SELENBP1 were 80% and 79% in discriminating NBE from preneoplastic lesions, 79% 
      and 82% in discriminating NBE from invasive LSCC, and 77% and 71% in 
      discriminating preneoplastic lesions from invasive LSCC, respectively. 
      Furthermore, knockdown of SELENBP1 in immortalized human bronchial epithelial 
      cell line 16HBE cells significantly increased the efficiency of B[a]P-induced 
      cell transformation. CONCLUSIONS: The present data shows for the first time that 
      decreased SELENBP1 is an early event in LSCC, increases B[a]P-induced human 
      bronchial epithelial cell transformation, and might serve as a novel potential 
      biomarker for early detection of LSCC.
FAU - Zeng, Gu-Qing
AU  - Zeng GQ
AD  - Key Laboratory of Cancer Proteomics of Chinese Ministry of Health, Xiangya 
      Hospital, Central South University, Changsha, Hunan, China ; School of Nursing, 
      University of South China, Hengyang, Hunan, China.
FAU - Yi, Hong
AU  - Yi H
FAU - Zhang, Peng-Fei
AU  - Zhang PF
FAU - Li, Xin-Hui
AU  - Li XH
FAU - Hu, Rong
AU  - Hu R
FAU - Li, Mao-Yu
AU  - Li MY
FAU - Li, Cui
AU  - Li C
FAU - Qu, Jia-Quan
AU  - Qu JQ
FAU - Deng, Xingming
AU  - Deng X
FAU - Xiao, Zhi-Qiang
AU  - Xiao ZQ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130819
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Proteome)
RN  - 0 (SELENBP1 protein, human)
RN  - 0 (Selenium-Binding Proteins)
SB  - IM
MH  - Amino Acid Sequence
MH  - Apoptosis
MH  - Bronchi/*pathology
MH  - Carcinoma, Squamous Cell/genetics/*metabolism/pathology
MH  - Cell Cycle
MH  - Cell Line, Tumor
MH  - Cell Transformation, Neoplastic/genetics/*metabolism
MH  - Down-Regulation
MH  - Epithelial Cells/metabolism/pathology
MH  - Gene Expression Regulation, Neoplastic
MH  - Gene Knockout Techniques
MH  - Humans
MH  - Laser Capture Microdissection
MH  - Lung Neoplasms/genetics/*metabolism/pathology
MH  - Molecular Sequence Data
MH  - Proteome/genetics/metabolism
MH  - ROC Curve
MH  - Respiratory Mucosa/pathology
MH  - Selenium-Binding Proteins/chemistry/*genetics/metabolism
MH  - Tandem Mass Spectrometry
PMC - PMC3747066
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2013/08/27 06:00
MHDA- 2014/04/09 06:00
PMCR- 2013/08/19
CRDT- 2013/08/27 06:00
PHST- 2013/06/05 00:00 [received]
PHST- 2013/07/11 00:00 [accepted]
PHST- 2013/08/27 06:00 [entrez]
PHST- 2013/08/27 06:00 [pubmed]
PHST- 2014/04/09 06:00 [medline]
PHST- 2013/08/19 00:00 [pmc-release]
AID - PONE-D-13-23245 [pii]
AID - 10.1371/journal.pone.0071865 [doi]
PST - epublish
SO  - PLoS One. 2013 Aug 19;8(8):e71865. doi: 10.1371/journal.pone.0071865. eCollection 
      2013.