Loss of human E-cadherin (ECD) correlated with invasiveness of transitional cell cancer in the renal pelvis, ureter and urinary bladder

Wakatsuki, Shunji; Watanabe, Ryusuke; Saito, Kazuhide; Saito, Toshiro; Katagiri, Atsuko; Sato, Shotaru; Tomita, Yoshihiko

doi:10.1016/0304-3835(96)04194-8

Cited by 41 publications

(29 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Upregulated E-cadherin in BFTC905 cells could explain the migration and invasion inhibition after TrkB blockade. Our study is consistent with a previous report which demonstrated the absence of E-cadherin protein and mRNA level in T24 cells (38). It may explain the weak inhibition of migration and the absence of inhibition on invasion in T24 cells after TrkB blockade.…”

Section: Discussionsupporting

confidence: 93%

TrkB antibody elicits cytotoxicity and suppresses migration/invasion of transitional cell carcinoma cells

Huang

Lai²,

Wu³

et al. 2010

Int J Oncol

View full text Add to dashboard Cite

Abstract. BDNF (brain-derived neurotrophic factor) and its receptor TrkB (tropomyosin receptor kinase B) play important roles in the progression of cancer, including transitional cell carcinoma (TCC) cells reported in our previous investigation. In this study, we used a specific TrkB antibody (Ab) to evaluate its effects on survival, proliferation and migration/ invasion in three TCC cell lines (BFTC905, T24 and TSGH8301) in vitro. The TrkB Ab at 1 and 3 μg/ml, but not the TrkA or TrkC Abs, significantly elicited cytotoxicity in TCC cells. The TrkB Ab at 3 μg/ml also induced apoptosis of TCC cells, which may result from up-regulation of phosphop38 plus down-regulation of survivin and securin expression. The TrkB Ab at 0.5 μg/ml, which did not show cytotoxicity, suppressed migration of TCC cells and invasion of BFTC905 cells, possibly mediated through increased E-cadherin, decreased BDNF-stimulated phospho-PLCÁ1 and reduced MMP-9 activity. These results indicate that TrkB blockade may be a new strategy for TCC therapy.

show abstract

Section: Discussionsupporting

confidence: 93%

TrkB antibody elicits cytotoxicity and suppresses migration/invasion of transitional cell carcinoma cells

Huang

Lai²,

Wu³

et al. 2010

Int J Oncol

View full text Add to dashboard Cite

show abstract

“…The role of adhesion molecules in UC is still controversial, and only a few studies have been published in the literature on this topic (6,10). Dysfunctions in cell-cell adhesion molecules have been related to the initial steps of tumor invasion and the development of metastasis in urothelial bladder carcinomas.…”

mentioning

confidence: 99%

Immune expression of E-cadherin and α, β and γ-Catenin adhesion molecules and prognosis for upper urinary tract urothelial carcinomas

et al. 2012

View full text Add to dashboard Cite

ARTIcLE INFO _________________________________________________________ ___________________Introduction: Cell adhesion molecules (CAM) are required for maintaining a normal epithelial phenotype, and abnormalities in CAM expression have been related to cancer progression, including bladder urothelial carcinomas. There is only one study that correlates E-cadherin and α-, β-and γ-catenin expression with prognosis of upper tract urothelial carcinomas. Our aim is to study the pattern of immune expression of these CAMs in urothelial carcinomas from the renal pelvis and ureter in patients who have been treated surgically. Our goal is to correlate these expression levels and characteristics with well-known prognostic parameters for disease-free survival. Materials and Methods: We evaluated specimens from 20 patients with urothelial carcinomas of the renal pelvis and ureter who were treated with nephroureterectomy or ureterectomy between June 1997 and January 2007. CAM expression was evaluated by immunohistochemistry in a tissue microarray and correlated with histopathological characteristics and patient outcomes after a mean follow-up of 55 months. Results: We observed a relationship between E-cadherin expression and disease recurrence. Disease recurrence occurred in 87.5% of patients with strong E-cadherin expression. Only 50.0% of patients with moderate expression and 0% of patients with weak or no expression of E-cadherin had disease recurrence (p = 0.014). There was also a difference in disease-free survival. Patients with strong E-cadherin expression had a mean disease-free survival rate of 49.1 months, compared to 83.9 months for patients with moderate expression (p = 0.011). Additionally, an absence of α-catenin expression was associated with tumors that were larger than 3 cm (p = 0.003). Conclusions: We demonstrated for the first time that immune expression of E-cadherin is related to tumor recurrence and disease-free survival rates, and the absence of α-catenin expression is related to tumor size in upper tract urothelial carcinomas.

show abstract

“…Decreased expression of the e-cadherin gene has been linked to aberrant methylation of this CpG island in several common forms of human cancer 8 -12 but, while E-Cad protein expression has been previously reported to be significantly decreased in bladder cancers, [13][14][15][16][17] no previously published study has investigated the potential role of methylation in causing loss of E-Cad expression in this form of cancer. Characterizing the extent of e-cadherin methylation in bladder cancer is of interest from the standpoint of understanding the pathogenesis of this disease, and also because aberrant methylation, detectable by sensitive, polymerase chain reaction-based methods, might be used as a marker for early detection of cancer in tissue and fluid specimens.…”

mentioning

confidence: 99%

Methylation of the E-cadherin Gene in Bladder Neoplasia and in Normal Urothelial Epithelium from Elderly Individuals

Bornman¹,

Mathew²,

Alsruhe³

et al. 2001

The American Journal of Pathology

111

View full text Add to dashboard Cite

Decreased expression of the epithelial cell adhesion protein E-Cadherin occurs in several forms of human epithelial-derived cancers, including bladder cancers.We investigated the possibility that aberrant methylation of the CpG island flanking the 5 transcriptional start site of the e-cadherin gene is responsible for the decreased expression of this gene in bladder cancer, similar to the relationship previously seen between e-cadherin methylation and gene expression in other types of human cancers. Using methylation-specific polymerase chain reaction , we found methylation of this CpG island in 20 of 47 cases (43%) of bladder neoplasms ranging from low-grade papillary neoplasms to advanced , invasive cancers. When methylation status was compared to immunochemical staining for E-Cadherin , we found significantly diminished levels of E-Cadherin expression in 14 of 15 cases (93%) with methylation of the gene. We also found decreased expression of E-Cadherin, although to a somewhat lesser extent, in a high percentage (77%) of the cases without methylation of the gene. Although these data suggest a relationship between e-cadherin CpG island methylation and decreased gene expression, it evident that other mechanisms also contribute to decreased expression of this gene in bladder neoplasia. Remarkably, we also found low levels of e-cadherin methylation in urothelial cells from three of nine (33%) histologically normal bladders, with all three of the normal bladder samples with methylated e-cadherin being from individuals older than 70 years of age. Thus, methylation of the e-cadherin CpG island may occur normally in this tissue with aging as well as in low-grade papillary neoplasms, and is not specific to cancer in the bladder. This finding of methylation in normal urothelial cells from elderly individuals is provocative with respect to a possible link between aging and increased risk for bladder cancer, but it suggests limitations on the usefulness of using methylation of e-cadherin as a molecular marker for detection of bladder cancer. (Am J Pathol 2001, 159:831-835)The E-Cadherin (E-Cad) transmembrane glycoprotein modulates calcium-dependent intercellular adhesion in a variety of epithelial tissues. The e-cadherin gene is mutated in the germline of some families with genetic predisposition to gastric cancers 1 and somatic mutations are common in lobular breast cancers and some gastric and gynecological cancers. [2][3][4] In many other common human cancers, including cancers of the breast, prostate, colon, stomach, esophagus, pancreas, thyroid, head and neck, and bladder, levels of E-Cad protein are greatly reduced compared to normal epithelial tissues. 5,6 The loss of ECad expression seems to be involved in invasive and metastatic properties of neoplastic cells, 7 consistent with the function of a tumor suppressor gene.The structure of the e-cadherin gene is notable for a dense CpG island that flanks the 5Ј transcriptional start site. Decreased expression of the e-cadherin gene has been linked to aberrant methylatio...

show abstract

Loss of human E-cadherin (ECD) correlated with invasiveness of transitional cell cancer in the renal pelvis, ureter and urinary bladder

Cited by 41 publications

References 13 publications

TrkB antibody elicits cytotoxicity and suppresses migration/invasion of transitional cell carcinoma cells

TrkB antibody elicits cytotoxicity and suppresses migration/invasion of transitional cell carcinoma cells

Immune expression of E-cadherin and α, β and γ-Catenin adhesion molecules and prognosis for upper urinary tract urothelial carcinomas

Methylation of the E-cadherin Gene in Bladder Neoplasia and in Normal Urothelial Epithelium from Elderly Individuals

Contact Info

Product

Resources

About