PMID- 20565895
OWN - NLM
STAT- MEDLINE
DCOM- 20100816
LR  - 20211020
IS  - 1471-2407 (Electronic)
IS  - 1471-2407 (Linking)
VI  - 10
DP  - 2010 Jun 19
TI  - 14-3-3epsilon contributes to tumour suppression in laryngeal carcinoma by 
      affecting apoptosis and invasion.
PG  - 306
LID - 10.1186/1471-2407-10-306 [doi]
AB  - BACKGROUND: 14-3-3epsilon regulates a wide range of biological processes, 
      including cell cycle control, proliferation, and apoptosis, and plays a 
      significant role in neurogenesis and the formation of malignant tumours. However, 
      the exact function and regulatory mechanism of 14-3-3epsilon in carcinogenesis 
      have not been elucidated. METHODS: The expression of 14-3-3epsilon was assessed 
      by RT-PCR and western blotting. The invasiveness and viability of Hep-2 cells 
      were determined by the transwell migration assay and MTT assay, respectively. 
      Cell cycle and apoptosis of Hep-2 cells were detected by flow cytometry. RESULTS: 
      The mRNA and protein expression of 14-3-3epsilon in larynx squamous cell 
      carcinoma (LSCC) tissues were significantly lower than those in clear surgical 
      margin tissues. Statistical analysis showed that the 14-3-3epsilon protein level 
      in metastatic lymph nodes was lower than that in paired tumour tissues. In 
      addition, the protein level of 14-3-3epsilon in stage III or IV tumours was 
      significantly lower than that in stage I or II tumours. Compared with control 
      Hep-2 cells, the percentages of viable cells in the 14-3-3epsilon-GFP and 
      negative control GFP groups were 36.68 +/- 14.09% and 71.68 +/- 12.10%, 
      respectively. The proportions of S phase were 22.47 +/- 3.36%, 28.17 +/- 3.97% 
      and 46.15 +/- 6.82%, and the apoptotic sub-G1 populations were 1.23 +/- 1.02%, 
      2.92 +/- 1.59% and 13.72 +/- 3.89% in the control, negative control GFP and 
      14-3-3epsilon-GFP groups, respectively. The percentages of the apoptotic cells 
      were 0.84 +/- 0.25%, 1.08 +/- 0.24% and 2.93 +/- 0.13% in the control, negative 
      control GFP and 14-3-3epsilon-GFP groups, respectively. The numbers of cells that 
      penetrated the filter membrane in the control, negative control GFP and 
      14-3-3epsilon-GFP groups were 20.65 +/- 1.94, 17.63 +/- 1.04 and 9.1 +/- 0.24, 
      respectively, indicating significant differences among the different groups. 
      CONCLUSIONS: Decreased expression of 14-3-3epsilon in LSCC tissues contributes to 
      the initiation and progression of LSCC. 14-3-3epsilon can promote apoptosis and 
      inhibit the invasiveness of LSCC.
FAU - Che, Xing-Hua
AU  - Che XH
AD  - Department of Medical Genetics, China Medical University, Heping District, 
      Shenyang, China.
FAU - Chen, Hong
AU  - Chen H
FAU - Xu, Zhen-Ming
AU  - Xu ZM
FAU - Shang, Chao
AU  - Shang C
FAU - Sun, Kai-Lai
AU  - Sun KL
FAU - Fu, Wei-Neng
AU  - Fu WN
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100619
PL  - England
TA  - BMC Cancer
JT  - BMC cancer
JID - 100967800
RN  - 0 (14-3-3 Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (YWHAE protein, human)
SB  - IM
MH  - 14-3-3 Proteins/genetics/*metabolism
MH  - *Apoptosis
MH  - Blotting, Western
MH  - Carcinoma, Squamous Cell/genetics/*metabolism/*prevention & control/secondary
MH  - Cell Line, Tumor
MH  - *Cell Movement
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Genes, Tumor Suppressor
MH  - Humans
MH  - Laryngeal Neoplasms/genetics/*metabolism/pathology/*prevention & control
MH  - Lymphatic Metastasis
MH  - Male
MH  - Middle Aged
MH  - Neoplasm Invasiveness
MH  - Neoplasm Staging
MH  - RNA, Messenger/metabolism
MH  - Recombinant Fusion Proteins/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - S Phase
MH  - Transfection
PMC - PMC2904731
EDAT- 2010/06/23 06:00
MHDA- 2010/08/17 06:00
PMCR- 2010/06/19
CRDT- 2010/06/23 06:00
PHST- 2010/01/16 00:00 [received]
PHST- 2010/06/19 00:00 [accepted]
PHST- 2010/06/23 06:00 [entrez]
PHST- 2010/06/23 06:00 [pubmed]
PHST- 2010/08/17 06:00 [medline]
PHST- 2010/06/19 00:00 [pmc-release]
AID - 1471-2407-10-306 [pii]
AID - 10.1186/1471-2407-10-306 [doi]
PST - epublish
SO  - BMC Cancer. 2010 Jun 19;10:306. doi: 10.1186/1471-2407-10-306.