PMID- 17982629
OWN - NLM
STAT- MEDLINE
DCOM- 20080123
LR  - 20151119
IS  - 1021-335X (Print)
IS  - 1021-335X (Linking)
VI  - 18
IP  - 6
DP  - 2007 Dec
TI  - Over-expression of 14-3-3sigma in budding colorectal cancer cells modulates cell 
      migration in the presence of tenascin-C.
PG  - 1451-6
AB  - Epigenetic silencing of the 14-3-3sigma gene by CpG hypermethylation has been 
      reported in many kinds of cancers, but has been considered inapplicable in the 
      colorectal variety. The expression of 14-3-3sigma in colorectal cancer is located 
      primarily in the invasive area. The interaction between tumor cells and the 
      extracellular matrix (ECM) is involved in tumor invasion. In the current study, 
      we investigated the correlation between 14-3-3sigma expression and the ECM, 
      focusing especially on the presence of tenascin-C (TNC) at the invasive area of 
      colorectal cancers. Correlations between the immunohistochemical expression of 
      14-3-3sigma and TNC, as well as other clinicopathological factors, were evaluated 
      in 123 colorectal carcinoma tissues. 14-3-3sigma expression was frequently 
      observed in budding tumor cells in the invasive area and expression was 
      significantly correlated with budding formation (p=0.001), pTNM classification 
      (p=0.001) and stromal TNC expression (p=0.004). Using colorectal cancer cell 
      lines and ECMs, the up-regulation of 14-3-3sigma mRNA levels was investigated by 
      semi-quantitative RT-PCR. TNC surrounding the tumor cells increased 14-3-3sigma 
      mRNA expression 1.8- to 2.2-fold in HCT116 cells. The effect of 14-3-3sigma 
      over-expression on tumor cell migration was investigated using an agarose-cell 
      droplet migration assay. Over-expression of 14-3-3sigma up-regulated HCT116 cell 
      migration on TNC (p<0.001). We concluded that the expression of 14-3-3sigma in 
      the invasive area modulates tumor cell migration in certain types of colorectal 
      cancer and thus facilitates tumor progression.
FAU - Ide, Munenori
AU  - Ide M
AD  - Department of General Surgical Science (Surgery I), Gunma University Graduate 
      School of Medicine, Gunma 371-8511, Japan. muide@showa.gunma-u.ac.jp
FAU - Saito, Kana
AU  - Saito K
FAU - Tsutsumi, Soichi
AU  - Tsutsumi S
FAU - Tsuboi, Kaori
AU  - Tsuboi K
FAU - Yamaguchi, Satoru
AU  - Yamaguchi S
FAU - Asao, Takayuki
AU  - Asao T
FAU - Kuwano, Hiroyuki
AU  - Kuwano H
FAU - Nakajima, Takashi
AU  - Nakajima T
LA  - eng
PT  - Journal Article
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (14-3-3 Proteins)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Tenascin)
RN  - EC 3.1.- (Exonucleases)
RN  - EC 3.1.- (Exoribonucleases)
RN  - EC 3.1.- (SFN protein, human)
SB  - IM
MH  - 14-3-3 Proteins
MH  - Biomarkers, Tumor/*metabolism
MH  - Cell Count
MH  - Cell Division
MH  - Cell Line, Tumor
MH  - Cell Movement
MH  - Colorectal Neoplasms/*metabolism/pathology/physiopathology/surgery
MH  - Exonucleases/*metabolism
MH  - Exoribonucleases
MH  - Humans
MH  - Immunohistochemistry
MH  - Lymphatic Metastasis/pathology
MH  - Neoplasm Invasiveness
MH  - Neoplasm Proteins/*metabolism
MH  - Neoplasm Staging
MH  - Tenascin/*metabolism
EDAT- 2007/11/06 09:00
MHDA- 2008/01/24 09:00
CRDT- 2007/11/06 09:00
PHST- 2007/11/06 09:00 [pubmed]
PHST- 2008/01/24 09:00 [medline]
PHST- 2007/11/06 09:00 [entrez]
PST - ppublish
SO  - Oncol Rep. 2007 Dec;18(6):1451-6.