Article Text

PDF
Reacquisition of E-cadherin expression in metastatic deposits of signet-ring cell carcinoma of the upper gastrointestinal system: a potential anchor for metastatic deposition
  1. Yihong R Ma,
  2. Gene P Siegal,
  3. Shi Wei
  1. Department of Pathology, The University of Alabama at Birmingham, Birmingham, Alabama, USA
  1. Correspondence to Dr Shi Wei, Department of Pathology, The University of Alabama at Birmingham, NP 3545A, 619 19th Street South, Birmingham, AL 35249-7331, USA; swei{at}uabmc.edu

Abstract

Aims To examine the expression of E-cadherin in paired primary and metastatic signet-ring cell carcinomas (SRCC) of various organ systems in order to explore the potential role of the molecule in metastatic dissemination of this unique tumour type.

Methods Thirty-seven consecutive cases of SRCC from various organs with paired primary and metastatic tumorous tissue available were retrieved. The intensity of membranous E-cadherin expression was semiquantitatively scored on a scale of 0–3+.

Results Reduced E-cadherin expression was a distinct feature of primary SRCC and was observed in 78% of primary tumours. Interestingly, the E-cadherin reduction was less frequently seen in metastatic SRCC when compared with their primary counterparts, and was only found in 57% of tumours in lymph node metastases or at distant sites of relapse. Furthermore, the mean score of E-cadherin expression of primary SRCC was significantly lower than that of their metastatic counterparts (2.3 vs 1.8; p=0.008). When divided by organ systems, the reacquisition of E-cadherin expression in the metastatic deposits was most remarkable in the SRCC of upper gastrointestinal tract origin (2.3 vs 1.4; p=0.003), whereas no significant difference was observed in other organ systems.

Conclusions While the reduction of E-cadherin in primary SRCC supports its pivotal role in epithelial-mesenchymal transition, a process crucial in tumour progression and metastatic dissemination, the re-expression of this molecule in metastatic SRCC cells implies a reversal to their epithelial phenotype (thus mesenchymal-epithelial transition) which, in turn, theoretically helps tumour cells to anchor and form cohesive metastatic deposits.

  • CARCINOMA
  • CELL ADHESION MOLECULES
  • GASTRIC CANCER

Statistics from Altmetric.com

Footnotes

  • This study was presented in part at the 2016 Annual Meeting of the American Society for Investigative Pathology in conjunction with Experimental Biology; 2–6 Apr 2016; San Diego, California, USA.

  • Handling editor Cheok Soon Lee

  • Competing interests None.

  • Ethics approval University of Alabama at Birmingham.

  • Provenance and peer review Not commissioned; externally peer reviewed.

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.