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Increased Expression of β-Catenin, Phosphorylated Glycogen Synthase Kinase 3β, Cyclin D1, and c-myc in Laterally Spreading Colorectal Tumors

Jing Wang¹, Xinying Wang¹, Wei Gong, Biantao Mi, Side Liu and Bo Jiang

Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China

Correspondence to: Dr Bo Jiang, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, 510515, Guangzhou, China. E-mail: drjiang{at}163.com

Laterally spreading tumors (LSTs) are considered a special subtype of superficial colorectal tumor. This study was performed to characterize the clinicopathological features and examine activation of the Wnt/β-catenin pathway in LSTs and protruded-type colorectal adenomas (PAs). Fifty LSTs and 54 PAs were collected, and their clinicopathological characteristics were compared. The expression of E-cadherin, β-catenin, glycogen synthase kinase-3β (GSK-3β), phosphorylated GSK-3β, (phospho-GSK-3β), cyclin D1, and c-myc was investigated by immunohistochemical staining on serial sections. Patients with LSTs were significantly older than those bearing PAs (63.4 vs 47.4 years old; p<0.001). The mean size of LSTs was significantly larger than that of PAs (27.0 mm vs 14.6 mm; p<0.01). Forty-eight percent of LSTs were located in the proximal colon, which was significantly higher than that of PAs (18.5%; p<0.05). Expression of β-catenin, phospho-GSK-3β, cyclin D1, and c-myc was significantly increased in LSTs compared with PAs (p<0.05). However, E-cadherin and total GSK-3β expression was not significantly different between the two groups. The level of β-catenin expression correlated strongly with phospho-GSK-3β, cyclin D1, and c-myc expression in LSTs but not in PAs. Our findings suggest that activation of the Wnt/β-catenin pathway is more prevalent in LSTs than in PAs, suggesting that phosphorylation-dependent inactivation of GSK-3β may be involved in LST carcinogenesis. (J Histochem Cytochem 57:363–371, 2009)

Key Words: laterally spreading colorectal tumor • carcinogenesis • Wnt/β-catenin pathway • GSK-3β • phosphorylation

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