scholarly journals microRNA-146a targets the L1 cell adhesion molecule and suppresses the metastatic potential of gastric cancer

2012 ◽  
Vol 6 (3) ◽  
pp. 501-506 ◽  
Author(s):  
ZHIBO HOU ◽  
HAITAO YIN ◽  
CONG CHEN ◽  
XINZHENG DAI ◽  
XIAOLIN LI ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Metastatic Potential ◽  
L1 Cell Adhesion Molecule

Role of L1 cell adhesion molecule in gastric carcinoma.

2011 ◽  
Vol 29 (4_suppl) ◽  
pp. 56-56
Author(s):  
T. Ito ◽  
Y. Kodera ◽  
C. Tanaka ◽  
N. Ohashi ◽  
G. Nakayama ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Adhesion ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Cell Line ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Parental Cell ◽  
Parental Cell Line ◽  
L1 Cell Adhesion Molecule

56 Background: L1 cell adhesion molecule (L1) is a 200-220 kDa transmembrane glycoprotein of the immunoglobulin super family initially identified in neural cells. L1 was detected in ovarian cancer in a stage-dependent manner, was found exclusively in the invasion front of colorectal cancer, and has been considered a stem cell marker in glioma. The authors have shown that mRNA expression of L1 was a significant prognostic factor in gastric cancer (Kodera et al. Gastrointestinal Cancer Symposium 2009, abst 37). Its role in gastric cancer was further investigated. Methods: Expression of L1 was observed by immunostaining in 72 surgically resected pT4A-stage gastric cancer specimens. The association of L1 with peritoneal seeding and prognosis was elucidated. mRNA expression of L1-expressing gastric cancer cell line, KATO3, was suppressed using siRNA (KATO3 L1-). Microarray was used to indentify molecules that differ in expression between KATO3 L1- and the parental cell line. Results: L1 was scarcely stained in non-cancerous epithelial cells and intestinal metaplastic cells. L1 was detected mainly in the cell surface membrane of cancer cells in 15 of 72 specimens, more often in the intestinal type cancer. No correlation was found between L1 expression and detection of cancer cells in the peritoneal washes or development of peritoneal carcinomatosis. Nevertheless, the prognosis of L1-positive cancer was significantly inferior (p = 0.024). Prognosis was particularly poor among 6 cases where L1 was expressed in cancer cells at the invasive front (median survival time 149 days). Of 40,000 genes evaluated in the microarray, mRNA expression of 50 genes were amplified by > 4-fold whereas the expression of 20 genes were attenuated to less than 1/4. Of these, expression of DYRK1A that induces apoptosis in conjunction with p53 was markedly suppressed to less than 1/8. Suppression of DYRK1A in the KATO3 L1- in comparison with the parental cell line was confirmed by RT-PCR. Conclusions: L1 affects prognosis of gastric cancer, particularly when it is expressed in cancer cells at the invasion front. Its role in the biology of gastric cancer has began to be elucidated. No significant financial relationships to disclose.

scholarly journals Semaphorin3D Regulates Axon Axon Interactions by Modulating Levels of L1 Cell Adhesion Molecule

2007 ◽  
Vol 27 (36) ◽  
pp. 9653-9663 ◽  
Author(s):  
M. A. Wolman ◽  
A. M. Regnery ◽  
T. Becker ◽  
C. G. Becker ◽  
M. C. Halloran
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
L1 Cell Adhesion Molecule

scholarly journals N-myc down regulates neural cell adhesion molecule expression in rat neuroblastoma.

1990 ◽  
Vol 10 (5) ◽  
pp. 2012-2016 ◽  
Author(s):  
R Akeson ◽  
R Bernards
Keyword(s):  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Neural Cell Adhesion Molecule ◽  
Neuroblastoma Cell ◽  
Metastatic Potential ◽  
Neural Cell ◽  
Human Neuroblastoma ◽  
Neuronal Markers ◽  
Neural Cell Adhesion

In human neuroblastoma, amplification of the N-myc oncogene is correlated with increased metastatic ability. We recently showed that transfection of the rat neuroblastoma cell line B104 with an N-myc expression vector resulted in an increase in metastatic ability and a significant reduction in the expression of major histocompatibility complex class I antigens. We examined whether N-myc causes additional phenotypic changes in these cells. We showed that expression of N-myc leads to a dramatic reduction in the levels of neural cell adhesion molecule (NCAM) polypeptides and mRNAs. Spontaneous revertants of the high N-myc phenotype were found to have regained significant levels of NCAM expression, indicating that the continued expression of N-myc is required to maintain the low NCAM phenotype. NCAM was not reduced in B104 cells transfected with the neomycin resistance vector alone, and other neuronal markers were not specifically reduced in N-myc-transfected B104 cells. As NCAM functions in cell-cell adhesion, decreased NCAM expression could contribute significantly to the increased metastatic potential of N-myc-amplified neuroblastomas.

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