[Correlation between the intercellular adhesion molecule (E-cadherin) and its associated protein (alpha-catenin) expression and metastasis in human digestive cancers].

H Shiozaki; J Gofuku; M Inoue; S Tamura

Home/Archive/PubMed

PubMed · 7629995

[Correlation between the intercellular adhesion molecule (E-cadherin) and its associated protein (alpha-catenin) expression and metastasis in human digestive cancers].

H Shiozaki·J Gofuku·M Inoue·S Tamura

View original source ↗Export metadata ↓

Abstract

The immunostaining (ABC method) of E-cadherin and alpha-catenin were performed on 46 esophageal cancers, 67 gastric cancers, 100 colon cancers. E-cadherin and alpha-catenin expression was evaluated as preserved and reduced according to the proportion of positive cells, respectively. The reduction of alpha-catenin expression was more significantly related to lymph node metastasis than that of E-cadherin. Furthermore, the frequency of hematogenous liver metastasis in preserved E-cadherin expression and reduced alpha-catenin expression was significantly higher than that in another combination of E-cadherin and alpha-catenin expression, in gastric and colon cancer. The reduction of alpha-catenin expression was associated with declined intercellular adhesiveness, which occasionally was not accompanied by reduction of E-cadherin. Therefore, the expression of alpha-catenin might more sensitively indicated cell-cell adhesion, predicting tumor metastasis.

Explore related subjects

Cadherins Colonic Neoplasms Cytoskeletal Proteins Digestive System Neoplasms Esophageal Neoplasms Humans Neoplasm Metastasis Stomach Neoplasms alpha Catenin English Abstract Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

H Shiozaki, J Gofuku, M Inoue, S Tamura. 1995. [Correlation between the intercellular adhesion molecule (E-cadherin) and its associated protein (alpha-catenin) expression and metastasis in human digestive cancers].. https://pubmed.ncbi.nlm.nih.gov/7629995/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

Allelic loss in a minimal region on chromosome 16q24 is associated with vitreous seeding of retinoblastoma.

In addition to RB1 gene mutations, retinoblastomas frequently show gains of 1q and 6p and losses of 16q. To identify suppressor genes on 16q, we analyzed 22 short tandem repeat loci in 58 patients with known RB1 mutations. A subset of tumors was also investigated by conventional and matrix comparative genomic hybridization. In 40 of 58 (69%) tumors, we found no loss of heterozygosity (LOH) at any 16q marker. LOH was detected in 18 of 58 (31%) tumors, including five with allelic imbalance at some markers. In one tumor LOH was only observed at 16q24. As the parental origin of allele loss was unbiased, an imprinted locus is unlikely to be involved. Analysis of gene expression by microarray hybridization and quantitative RT real-time PCR did not identify a candidate suppressor in 16q24. Cadherin 13 (CDH13), CBFA2T3, and WFDC1, which are candidate suppressors in other tumor entities with 16q24 loss, did not show loss of expression. In addition, mutation and methylation analysis showed no somatic alteration of CDH13. Results in all tumors with chromosome 16 alterations define a single minimal deleted region of 5.7 Mb in the telomeric part of 16q24 with the centromeric boundary defined by retention of heterozygosity for a single nucleotide variant in exon 10 of CDH13 (Mb 82.7). Interestingly, clinical presentation of tumors with and without 16q alterations was distinct. Specifically, almost all retinoblastomas with 16q24 loss showed diffuse intraocular seeding. This suggests that genetic alterations in the minimal deleted region are associated with impaired cell-to-cell adhesion.

Cadherins↗

PubMed2007

Expression of E-cadherin and its repressor snail in placental tissue of normal, preeclamptic and HELLP pregnancies.

Incomplete invasion of extravillous trophoblasts (EVT) is thought to be associated with complications of pregnancy. Snail, a zinc-finger transcription factor represses the transcription of the cell adhesion molecule E-cadherin. The aim of this study was to investigate the expression of E-cadherin and Snail in placental tissue with preeclampsia or HELLP. Placental tissues were obtained from five patients with HELLP syndrome, seven patients with preeclampsia and seven patients after a normal term birth and analysed for Snail and E-cadherin immunoreactivity with specific monoclonal antibodies. Immunohistochemical staining of the placental tissue was analysed using an immunoreactivity score for the evaluation of staining intensity. In preeclamptic EVT, Snail immunoreactivity showed a significant 1.7-fold increase, accompanied by a significant 1.9-fold reduction of E-cadherin immunoreactivity. A 1.7-fold increase of Snail and in parallel a 1.3-fold reduction of E-cadherin was observed in EVT of HELLP placentas although without statistical significance. Loss of E-cadherin can be observed during epithelial-mesenchymal transition (EMT), a key process in normal development and trophoblast differentiation. Snail represses the transcription of E-cadherin triggering a complete EMT. Results obtained in this study showed changes of Snail and E-cadherin immunoreactivity in preeclamptic placentas that could be accompanied with an altered EMT in trophoblasts.

Cadherins↗

PubMed2007

Congenital self-healing reticulohistiocytosis (Hashimoto-Pritzker disease): ten-year experience at Dallas Children's Medical Center.

The real incidence of congenital self-healing reticulohistiocytosis (CSHR) may be underreported because of its high rate of spontaneous resolution and lack of clinical recognition. Currently, there are no criteria other than clinical that can reliably distinguish CSHR from cutaneous involvement by disseminated Langerhans cell histiocytosis (LCH). In this study we investigate the role of E-cadherin, Ki-67, and phosphorylated histone H3 (PHH3) immunohistochemical stains in distinguishing CSHR from disseminated LCH. We found that no significant difference was seen in the histologic features and the expression of E-cadherin, Ki-67, and PHH3 between the two groups; thus supporting the theory that CSHR and LCH represent different ends of a spectrum of the same condition.

Cadherins↗