Key result
GKLF transcript levels were lower in 14 of 17 esophageal squamous cell carcinomas compared to normal mucosa, and antisense GKLF transfection increased cancer cell proliferation (P<0.05).
GKLF is down-regulated in esophageal squamous cell carcinoma, and its suppression in vitro increases cell proliferation and decreases adhesion, suggesting a tumor suppressor role.
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Supports GKLF as tumor suppressor in esophageal cancer models; leaves open therapeutic targeting pending human validation.
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.
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Nan Wang (2002) studied Esophageal squamous cell carcinoma (n=17). GKLF expression and antisense GKLF transfection vs. Paired normal mucosa and vector transfected cell control was evaluated on GKLF transcript level, cell proliferation rate, and adhesion ability (p=<0.05). GKLF transcript levels were lower in 14 of 17 esophageal squamous cell carcinomas compared to normal mucosa, and antisense GKLF transfection increased cancer cell proliferation (P<0.05).
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