Effects of E-cadherin (CDH1) gene promoter polymorphisms on the risk and clinicopathologic development of oral cancer

Head & Neck ◽  
2011 ◽  
Vol 34 (3) ◽  
pp. 405-411 ◽  
Author(s):  
Ming-Hsien Chien ◽  
Lin Shih-Shen Chou ◽  
Tsung-Te Chung ◽  
Chien-Huang Lin ◽  
Ming-Yung Chou ◽  
...  
2011 ◽  
Vol 104 (3) ◽  
pp. 299-304 ◽  
Author(s):  
Ming-Hsien Chien ◽  
Kun-Tu Yeh ◽  
Yi-Ching Li ◽  
Yi-Hsien Hsieh ◽  
Chien-Huang Lin ◽  
...  

2006 ◽  
Vol 175 (4S) ◽  
pp. 198-198
Author(s):  
Lambertus A. Kiemeney ◽  
Kjeld P. Van Houwelingen ◽  
Manon Bogaerts ◽  
J. Alfred Witjes ◽  
Dorine W. Swinkels ◽  
...  

2011 ◽  
Vol 27 (2) ◽  
pp. 151-158 ◽  
Author(s):  
Yadong Wang ◽  
Haiyan Yang ◽  
Li Li ◽  
Haiyu Wang ◽  
Congke Zhang ◽  
...  

Reproduction ◽  
2007 ◽  
Vol 134 (2) ◽  
pp. 373-378 ◽  
Author(s):  
Kang Shan ◽  
Ma Xiao-Wei ◽  
Wang Na ◽  
Zhang Xiu-Feng ◽  
Wen Deng-Gui ◽  
...  

Endometriosis, one of the most frequent diseases in gynecology, is a benign but invasive and metastatic disease. The altered expression of E-cadherin may play an important role in developing endometriosis. In this paper, we discuss the association of three single nucleotide polymorphisms (SNPs) on the E-cadherin gene and risk of endometriosis. We examined the genotype frequency of three polymorphisms in 152 endometriosis patients and 189 control women. There was a significant difference in the frequency of the E-cadherin 3′-UTR C → T genotypes between endometriosis and controls (P = 0.01). The frequency of the C allele in patients (71.1%) was significantly higher than in the controls (63.8%; P = 0.04). When compared with the T/T + T/C genotypes, the C/C genotype had a significantly increased susceptibility to endometriosis, with an adjusted odds ratio of 1.79 (95% confidence interval = 1.17–2.76). No significant difference was found between endometriosis and control women on two polymorphisms (−160 C → A, −347 G → GA) at the gene promoter region of E-cadherin. The −160 C → A and −347 G → GA polymorphisms displayed linkage disequilibrium (D′ = 0.999). The −160 A/−347 GA haplotype was only detected in endometriosis patients (2%). These data show a relation between the E-cadherin 3′-UTR C → T polymorphism, the −160 A/−347 GA haplotype of two promoter polymorphisms and risk of endometriosis, suggesting a potential role in endometriosis development, at least in North Chinese women.


2006 ◽  
Vol 163 (suppl_11) ◽  
pp. S110-S110
Author(s):  
L Kiemeney ◽  
K van Houwelingen ◽  
M Bogaerts ◽  
A Witjes ◽  
D Swinkels ◽  
...  

2006 ◽  
Vol 42 (18) ◽  
pp. 3219-3227 ◽  
Author(s):  
Lambertus A. Kiemeney ◽  
Kjeld P. van Houwelingen ◽  
Manon Bogaerts ◽  
J. Alfred Witjes ◽  
Dorine W. Swinkels ◽  
...  

2014 ◽  
Vol 14 (2) ◽  
pp. 115-127 ◽  
Author(s):  
G. Pannone ◽  
A. Santoro ◽  
A. Feola ◽  
P. Bufo ◽  
P. Papagerakis ◽  
...  

Author(s):  
Islam Mohamed ◽  
Ahmed Moahmed ◽  
Mennatallah Abdelkader ◽  
Alaaeldin Saleh ◽  
Ala-Eddin Al-Moustafa

Introduction: Elaeagnus angustifolia (EA) is a medicinal plant that has been used for centuries in treating many human diseases, in the Middle East, including fever, amoebic dysentery, gastrointestinal problems. However, the effect of EA plant extract on human cancer progression especially oral malignancy has not been investigated yet. Thus, first we examined the effect of EA flower extract on angiogenesis in ovo, and on selected parameters in human oral cancer cells. Materials and methods: Chorioallantoic membranes (CAMs) of chicken embryos at 3-7 days of incubation were used to assess the effect EAflower plant extract on angiogenesis. Meanwhile, cell proliferation, soft agar, cell cycle, cell invasion and cell wounding assays were performed to explore the outcome of EA plant extract on FaDu and SCC25 oral cancer cell lines. On the other hand, western blot analysis was carried out to evaluate E-cadherin and Erk1/Erk2 expression and activation, respectively, in FaDu and SCC25 under the effect of EA extract. Results: Our data show that EA extract inhibits cell proliferation and colony formation, in addition to the initiation of Scell cycle arrest and reductionof G1/G2 phases. In parallel, EA extract provokes differentiation to an epithelial phenotype “mesenchymal-epithelial transition: MET” which is the opposite of “epithelial-mesenchymal transition, EMT”: an important event in cell invasion and metastasis. Thus, EA extract causes a dramatic decrease in cell motility and invasion abilities of FaDu and SCC25 cancer cells in comparison with their controls. These changes are accompanied by an up-regulation of E-cadherin expression. The molecular pathway analysis of the EA flower extract reveals that it can inhibit the phosphorylation of Erk1/Erk2, which could be behind the inhibition of angiogenesis, the initiation of MET event and the overexpression of E-cadherin. Conclusions: Our findings indicate that EA plant extract can downgrade human oral cancer progression by the inhibition of angiogenesis and cell invasion via Erk1/Erk2 signaling pathways.


Author(s):  
Danyal Imani ◽  
Navid Dashti ◽  
Arash Parvari ◽  
Sajad Shafiekhani ◽  
Fatemeh Alebrahim ◽  
...  

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