Peng Wang1, Li Li2, Ting Li3. 1. Department of Clinical Laboratory, Lishui People's Hospital (6th Affiliated Hospital of Wenzhou Medical University), Lishui 323000, Zhejiang, P.R. China. 2. Department of Pathology, Jiangsu Province Hospital of TMC, Jiangsu 210029, P.R. China. 3. Department of Oncology, Lishui People's Hospital (6th Affiliated Hospital of Wenzhou Medical University), Lishui 323000, Zhejiang, P.R. China.
Abstract
OBJECTIVES: To analyze the relationship between cysteine-rich 61 (Cyr61) and target genes of Wnt/β-catenin pathway (CCND1 and MYC) in 40 esophageal squamous cell carcinoma (ESCC) tissue specimens. Another aim of this study was to verify whether Cyr61 could be regulated by Wnt/β-catenin signaling. MATERIALS AND METHODS: Forty ESCC tissue specimens with paired adjacent normal epithelial tissues were obtained. The expression of Cyr61, CCND1, and MYC was examined by quantitative real-time polymerase chain reaction. Regression analysis was further performed to evaluate the correlation between expression levels of Cyr61 and CCND1, MYC. Finally, the mRNA expression of Cyr61 was determined in ESCC cells after lithium chloride (LiCl) treatment, which activated intrinsic Wnt/β-catenin signaling. RESULTS: Cyr61, CCND1, and MYC were obviously increased in ESCC tissue specimens than the matched normal epithelial tissues. Positive correlation of Cyr61 expression with CCND1 and/or MYC was validated by regression analysis. In addition, the expression of Cyr61 could be modulated by LiCl, an activator of Wnt/β-catenin signaling. CONCLUSION: Our data characterized that Cyr61 was aberrantly upregulated in ESCC tissues and was positively correlated to the targets of Wnt/β-catenin pathway. We also speculated that Cyr61 might be a direct target of this pathway and play a crucial role in ESCC progression.
OBJECTIVES: To analyze the relationship between cysteine-rich 61 (Cyr61) and target genes of Wnt/β-catenin pathway (CCND1 and MYC) in 40 esophageal squamous cell carcinoma (ESCC) tissue specimens. Another aim of this study was to verify whether Cyr61 could be regulated by Wnt/β-catenin signaling. MATERIALS AND METHODS: Forty ESCC tissue specimens with paired adjacent normal epithelial tissues were obtained. The expression of Cyr61, CCND1, and MYC was examined by quantitative real-time polymerase chain reaction. Regression analysis was further performed to evaluate the correlation between expression levels of Cyr61 and CCND1, MYC. Finally, the mRNA expression of Cyr61 was determined in ESCC cells after lithium chloride (LiCl) treatment, which activated intrinsic Wnt/β-catenin signaling. RESULTS:Cyr61, CCND1, and MYC were obviously increased in ESCC tissue specimens than the matched normal epithelial tissues. Positive correlation of Cyr61 expression with CCND1 and/or MYC was validated by regression analysis. In addition, the expression of Cyr61 could be modulated by LiCl, an activator of Wnt/β-catenin signaling. CONCLUSION: Our data characterized that Cyr61 was aberrantly upregulated in ESCC tissues and was positively correlated to the targets of Wnt/β-catenin pathway. We also speculated that Cyr61 might be a direct target of this pathway and play a crucial role in ESCC progression.