論文 - 詳細
| RRC ID | 18238 |
|---|---|
| 著者 | Xu H, Inagaki Y, Seyama Y, Hasegawa K, Sugawara Y, Du G, Wang F, Tang W, Kokudo N. |
| タイトル | Expression of KL-6/MUC1 in pancreatic ductal carcinoma and its potential relationship with β-catenin in tumor progression. |
| ジャーナル | Life Sci |
| Abstract |
AIM:The aim of this study was to evaluate the expression of Krebs yon den Lundgen-6/Mucin 1 (KL-6/MUC1) in pancreatic ductal carcinoma and its potential relationship with β-catenin in tumor progression. MAIN METHODS:The expressions of KL-6/MUC1 and β-catenin in 18 cases of pancreatic ductal carcinoma were detected by immunohistochemical staining. To determine the impact of KL-6/MUC1 down-regulation on pancreatic ductal carcinoma progression, siRNA targeting MUC1 was used to knockdown KL-6/MUC1 expression. The down-regulation of KL-6/MUC1 expression was confirmed by reverse transcription-polymerase chain reaction and immunofluorescence staining. E-cadherin and E-cadherin/β-catenin complex expressions were determined by immunoprecipitation. The expressions of KL-6/MUC1, β-catenin, cyclin D1 and c-myc were detected by Western blot. Cell proliferation, apoptosis and invasive abilities were detected by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide assay, Annexin V-FITC apoptosis detection kit and invasion assay. KEY FINDINGS:Positive KL-6/MUC1 staining was observed in the cancer tissues of all the 18 pancreatic ductal carcinoma cases (100.0%), and high nuclear β-catenin expression was seen in 12 cancers (66.7%). Reverse transcription-polymerase chain reaction and immunofluorescence staining showed that both KL-6/MUC1 mRNA and protein were effectively silenced by MUC1 siRNA. After KL-6/MUC1 knockdown, E-cadherin and E-cadherin/β-catenin complex expressions were increased, while the nuclear β-catenin, cyclin D1, and c-myc expressions were decreased. Down-regulation of KL-6/MUC1 also resulted in slower proliferation, increased apoptosis and decreased invasive ability. SIGNIFICANCE:This study indicated that KL-6/MUC1 played a complex role in regulating pancreatic ductal carcinoma cell proliferation, apoptosis, and invasion, and also supported the hypothesis that there is a functional link between KL-6/MUC1 expression and β-catenin subcellular localization. |
| 巻・号 | 88(23-24) |
| ページ | 1063-9 |
| 公開日 | 2011-6-6 |
| DOI | 10.1016/j.lfs.2011.03.021 |
| PII | S0024-3205(11)00158-5 |
| PMID | 21466814 |
| MeSH | Aged Aged, 80 and over Apoptosis / genetics Blotting, Western Carcinoma, Pancreatic Ductal / genetics* Carcinoma, Pancreatic Ductal / pathology Cell Proliferation Disease Progression Female Fluorescent Antibody Technique Gene Expression Regulation, Neoplastic* Humans Immunoprecipitation Male Middle Aged Mucin-1 / genetics* Neoplasm Invasiveness Pancreatic Neoplasms / genetics* Pancreatic Neoplasms / pathology Reverse Transcriptase Polymerase Chain Reaction beta Catenin / metabolism* |
| IF | 3.647 |
| 引用数 | 5 |
| WOS 分野 | MEDICINE, RESEARCH & EXPERIMENTAL PHARMACOLOGY & PHARMACY |
| リソース情報 | |
| ヒト・動物細胞 | PANC-1(RCB2095) |