PMID- 22815795
OWN - NLM
STAT- MEDLINE
DCOM- 20130321
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 7
IP  - 7
DP  - 2012
TI  - Decreased expression of SATB2: a novel independent prognostic marker of worse 
      outcome in laryngeal carcinoma patients.
PG  - e40704
LID - 10.1371/journal.pone.0040704 [doi]
LID - e40704
AB  - BACKGROUND: To investigate the expression and role of special AT-rich 
      sequence-binding protein-2 (SATB2) in laryngeal squamous cell carcinoma (LSCC) 
      tissue and cell line (HEp2), and to evaluate the clinical and prognostic 
      significance of SATB2 protein in patients with LSCC. METHODS: The expression of 
      SATB2 was examined in LSCC tissue and HEp2 cells by Western-blotting, Real-time 
      PCR and immunohistochemical staining. Cell growth curve assay and colony 
      formation assay were used to verify the effect of SATB2 on the proliferation and 
      tumor progression ability of HEp2 cells. Tumor formation assay in nude mice was 
      used to analyze the effect of SATB2 on the tumorigenicity of HEp2 cells. RESULTS: 
      The status of SATB2 protein in carcinoma tissues is much lower than that in 
      paracarcinoma tissues. The overall survival of the patients with high SATB2 
      expression was significantly higher than the low SATB2 expression group. Lower or 
      negative SATB2 expression was significantly correlated with advanced clinical 
      staging, histological grade and tumor recurrence. In vitro experiments 
      demonstrated that over-expression of SATB2 in HEp2 cells inhibited cell 
      proliferation and tumor progression ability, and down-regulation of SATB2 showed 
      the opposite effects. Over-expression of SATB2 repressed the tumorigenicity of 
      HEp2 cells by in vivo experiments. Moreover, multivariate analysis suggested that 
      SATB2 expression might be an independent prognostic indicator for the survival of 
      LSCC patients after curative surgery. CONCLUSIONS: SATB2 might involve in the 
      development and progression of LSCC as a tumor suppressor, and thereby may be a 
      valuable prognostic marker for LSCC patients.
FAU - Liu, Tian-Run
AU  - Liu TR
AD  - State Key Laboratory of Oncology in South China, Guangzhou, Guangdong, People's 
      Republic of China.
FAU - Xu, Li-Hua
AU  - Xu LH
FAU - Yang, An-Kui
AU  - Yang AK
FAU - Zhong, Qian
AU  - Zhong Q
FAU - Song, Ming
AU  - Song M
FAU - Li, Man-Zhi
AU  - Li MZ
FAU - Hu, Li-Juan
AU  - Hu LJ
FAU - Chen, Fu-Jin
AU  - Chen FJ
FAU - Hu, Ze-Dong
AU  - Hu ZD
FAU - Han, Ping
AU  - Han P
FAU - Zeng, Mu-Sheng
AU  - Zeng MS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120716
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Matrix Attachment Region Binding Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (SATB2 protein, human)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Aged
MH  - Animals
MH  - Biomarkers, Tumor/*genetics
MH  - Carcinoma, Squamous Cell/genetics/pathology
MH  - Cell Line, Tumor
MH  - Cell Proliferation
MH  - Disease Progression
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Immunohistochemistry
MH  - Laryngeal Neoplasms/*genetics/pathology
MH  - Matrix Attachment Region Binding Proteins/*genetics/metabolism
MH  - Mice
MH  - Mice, Nude
MH  - Middle Aged
MH  - Prognosis
MH  - Proportional Hazards Models
MH  - RNA, Messenger/genetics/metabolism
MH  - Survival Analysis
MH  - Transcription Factors/*genetics/metabolism
MH  - Treatment Outcome
PMC - PMC3398043
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2012/07/21 06:00
MHDA- 2013/03/22 06:00
PMCR- 2012/07/16
CRDT- 2012/07/21 06:00
PHST- 2012/02/16 00:00 [received]
PHST- 2012/06/12 00:00 [accepted]
PHST- 2012/07/21 06:00 [entrez]
PHST- 2012/07/21 06:00 [pubmed]
PHST- 2013/03/22 06:00 [medline]
PHST- 2012/07/16 00:00 [pmc-release]
AID - PONE-D-12-04703 [pii]
AID - 10.1371/journal.pone.0040704 [doi]
PST - ppublish
SO  - PLoS One. 2012;7(7):e40704. doi: 10.1371/journal.pone.0040704. Epub 2012 Jul 16.