Dataset Information

Down-regulation of gut-enriched Kruppel-like factor expression in esophageal cancer.

ABSTRACT: AIM:Esophageal carcinoma is one of the most common malignant tumors in China. But the molecular mechanisms of esophageal carcinoma remains unclear. Gut-enriched Kruppel-like factor (GKLF) is a newly identified transcription factor which is expressed abandantly in the epithelial cells of the gastrointestinal tract and deregulation of GKLF was linked to several types of cancer. It is of interest to study the expression and role of GKLF in esophageal carcinoma. METHODS:Semi-quantitative RT-PCR was used to compare GKLF expression in esophageal squamous cell carcinoma to normal mucosa of the same patients. The serum deprivation inducibility of GKLF was observed in an esophageal squamous cancer cell line by comparison to the primary culture of human fibroblast. The effect of antisense GKLF transfection on the proliferation and adhesion of esophageal squamous cancer cell line was also observed. RESULTS:The level of GKLF transcript is lower in esophageal squamous cell carcinoma compared to paired normal-appearing mucosa in 14 of 17 of the tumors analyzed. The serum deprivation inducibility of GKLF was greatly decreased in an esophageal squamous cancer cell line compared to the primary culture of human fibroblast. Decreased expression of GKLF in the esophageal cancer cell by antisense GKLF transfection increased its proliferation rate compared with that of vector transfected cell control (P<0.05). Transfection of antisense GKLF decreased its adhesion ability (P<0.05). CONCLUSION:The findings of this study demonstrate the down-regulation of GKLF in esophageal squamous cancer, and suggest that deregulation of GKLF may play a role in initiation and/or progression as well as the metastasis of esophageal squamous cancer.

SUBMITTER: Wang N

PROVIDER: S-EPMC4656400 | biostudies-literature | 2002 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Down-regulation of gut-enriched Kruppel-like factor expression in esophageal cancer.

Wang Nan N Liu Zhi-Hua ZH Ding Fang F Wang Xiu-Qin XQ Zhou Chuan-Nong CN Wu Min M

World journal of gastroenterology 20021201 6

<h4>Aim</h4>Esophageal carcinoma is one of the most common malignant tumors in China. But the molecular mechanisms of esophageal carcinoma remains unclear. Gut-enriched Kruppel-like factor (GKLF) is a newly identified transcription factor which is expressed abandantly in the epithelial cells of the gastrointestinal tract and deregulation of GKLF was linked to several types of cancer. It is of interest to study the expression and role of GKLF in esophageal carcinoma.<h4>Methods</h4>Semi-quantitat ...[more]

PMID: 12439907

Similar Datasets

Project description:To evaluate the significance of ?-catenin in clinical pathology, cellular function and signaling mechanism in esophageal squamous cell carcinoma (ESCC).The mRNA expression of ?-catenin was detected by real-time quantitative reverse transcription-polymerase chain reaction in 95 tissue specimens and evaluated for association with the clinicopathologic characteristics and survival time of patients with ESCC. siRNAs against human ?-catenin were used to inhibit ?-catenin expression. Hanging drop aggregation assay and dispase-based dissociation assay were performed to detect the effect of ?-catenin on ESCC cell-cell adhesion. Transwell assay was performed to determine cell migration. Luciferase-based transcriptional reporter assay (TOPflash) was used to measure ?-catenin-dependent transcription in cells with reduced ?-catenin expression. The expression and subcellular localizations of ?-catenin and E-cadherin were examined using Western blot and immunofluorescence analysis.?-catenin mRNA expression was significantly associated with tumor histological grade (P = 0.017) in ESCC. Kaplan-Meier survival analysis showed that ?-catenin expression levels had an impact on the survival curve, with low ?-catenin indicating worse survival (P = 0.003). The multivariate Cox regression analysis demonstrated that ?-catenin was an independent prognostic factor for survival. Experimentally, silencing ?-catenin caused defects in cell-cell adhesion and a concomitant increase in cell migration in both KYSE150 and TE3 ESCC cells. Analysis of Wnt signaling revealed no activation event associated with ?-catenin expression. Total ?-catenin and Triton X-100-insoluble ?-catenin were significantly reduced in the ?-catenin-specific siRNA-transfected KYSE150 and TE3 cells, whereas Triton X-100-soluble ?-catenin was not altered. Moreover, knocking down ?-catenin expression resulted in a significant decrease of E-cadherin and Triton X-100-insoluble desmocollin-2, along with reduced ?-catenin and E-cadherin membrane localization in ESCC cells.?-catenin is a tumor suppressor in ESCC and may serve as a prognostic marker. Dysregulated expression of ?-catenin may play important roles in ESCC progression.

Dataset Information

Down-regulation of gut-enriched Kruppel-like factor expression in esophageal cancer.

Publications

Down-regulation of gut-enriched Kruppel-like factor expression in esophageal cancer.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets