Conversion of cadherin isoforms in cultured human gastric carcinoma cells

• Published in: World journal of gastroenterology : WJG Vol. 12; no. 6; pp. 966 - 970
• Main Authors: Wang, Bing-Jing, Zhang, Zhi-Qian, Ke, Yang
• Format: Journal Article
• Language: English
• Published: United States Beijing Institute for Cancer Research and School of Oncology,Peking University,Beijing 100034,China 14.02.2006; Baishideng Publishing Group Co., Limited
• Subjects: Cadherins - genetics; Cadherins - metabolism; Cell Line, Tumor; DNA Primers; Humans; Protein Isoforms - genetics; Protein Isoforms - metabolism; Rapid Communication; Reverse Transcriptase Polymerase Chain Reaction; Stomach Neoplasms - pathology; Transcription Factors - metabolism; 人工培养; 对碘氧基苯甲醚; 肿瘤细胞; Transcription factor; N-cadherin; E-cadherin; Gastric cancer
• ISSN: 1007-9327; 2219-2840
• DOI: 10.3748/wjg.v12.i6.966

AIM： To explore the expression of cadherin isoforms in cultured human gastric carcinoma cells and its regulation. METHODS： The expressions of cell adhesion molecules （including E-cadherin, N-cadherin, α-catenin, β-catenin） and cadherin transcription factors including snail, slug and twist were determined by reverse transcriptasepolymerase chain reaction（RT-PCR）, immunoblotting and immunofluorescence in SV40-immortalized human gastric cell line Ges-1 and human gastric cancer cell lines MGC-803, BGC-823 and SGC-7901. RESULTS： All cell lines expressed N-cadherin, but not E-cadherin. N-cadherin immunofluorescence was detected at cell membranous adherents junctions where co-localization with immunofluorescent staining of inner surface adhesion proteins α- and β-catenins was observed. The transformed Ges-1 and gastric cancer cell lines all expressed transcription factors （snail, slug and twist） which inhibited the expression of E-cadherin and triggered epithelial-mesenchymal transformation. CONCLUSION： Cadherin isoforms can change from E-cadherin to N-cadherin in transformed human gastric cancer cells, which is associated with intracellular events of stomach carcinogenesis and high expression of corresponding transcription factors.