BACKGROUND: Although E-cadherin and beta-catenin are key regulators in tumor invasion and proliferation, few studies have been undertaken on the expression of these genes at the messenger ribonucleic acid (mRNA) level in relation to the progression of colon cancer. PATIENTS AND METHODS: In this study, tissue samples from colectomy (n = 37) or hepatectomy (n = 23) were collected in both tumor and adjacent normal tissues. Real-time quantitative reverse transcriptase-polymerase chain reaction was used to quantify E-cadherin and beta-catenin mRNAs in reference to 18S RNA. RESULTS: E-cadherin and beta-catenin levels in colon carcinomas were not statistically different compared with adjacent normal mucosa and were not correlated with tumor, nodes, and metastases (TNM) stage. Conversely, E-cadherin and beta-catenin levels were significantly higher in liver metastases than in adjacent normal tissue. Interestingly, we found that E-cadherin level in liver metastases was correlated to the TNM stage of the related primary tumor: a higher E-cadherin level was found for State I-II TNM. In addition, a high expression of E-cadherin in liver metastases was associated with a lower occurrence of extra-hepatic metastases after resection of liver metastases. CONCLUSION: Taken together, these data show that E-cadherin and beta-catenin expressions are regulated throughout colon cancer progression.
BACKGROUND: Although E-cadherin and beta-catenin are key regulators in tumor invasion and proliferation, few studies have been undertaken on the expression of these genes at the messenger ribonucleic acid (mRNA) level in relation to the progression of colon cancer. PATIENTS AND METHODS: In this study, tissue samples from colectomy (n = 37) or hepatectomy (n = 23) were collected in both tumor and adjacent normal tissues. Real-time quantitative reverse transcriptase-polymerase chain reaction was used to quantify E-cadherin and beta-catenin mRNAs in reference to 18S RNA. RESULTS:E-cadherin and beta-catenin levels in colon carcinomas were not statistically different compared with adjacent normal mucosa and were not correlated with tumor, nodes, and metastases (TNM) stage. Conversely, E-cadherin and beta-catenin levels were significantly higher in liver metastases than in adjacent normal tissue. Interestingly, we found that E-cadherin level in liver metastases was correlated to the TNM stage of the related primary tumor: a higher E-cadherin level was found for State I-II TNM. In addition, a high expression of E-cadherin in liver metastases was associated with a lower occurrence of extra-hepatic metastases after resection of liver metastases. CONCLUSION: Taken together, these data show that E-cadherin and beta-catenin expressions are regulated throughout colon cancer progression.
Authors: Elena Theophanous; Constantina Petraki; Andreas Scorilas; Vassilios Komborozos; George Veloudis; Jozsef L Varga; Marta Zarandi; Andrew V Schally; Michael Koutsilieris Journal: Mol Med Date: 2009-04-15 Impact factor: 6.354
Authors: Aleksandra Stanczak; Rafal Stec; Lubomir Bodnar; Wojciech Olszewski; Marzena Cichowicz; Wojciech Kozlowski; Cezary Szczylik; Tadeusz Pietrucha; Maciej Wieczorek; Monika Lamparska-Przybysz Journal: Pathol Oncol Res Date: 2011-06-16 Impact factor: 3.201