Association of Wnt1/β-Catenin with Clinical Pathological Characteristics and Prognosis of Esophageal Squamous Cell Carcinoma

Abstract

The aim of this study was to investigate the correlation between Wnt1=b-catenin expression and the clinicopathologic features and prognosis of patients with esophageal squamous cell carcinoma (ESCC). The mRNA and protein expression levels of Wnt1=b-catenin genes in 70 ESCC and 15 adjacent noncancerous paraffin-embedded samples were determined by real-time quantitative polymerase chain reaction and immunohistochemical staining. The mRNA expression level of Wnt1=b-catenin in ESCC was significantly higher than that in the adjacent noncancerous tissues (1.9934 AE 1.9888 vs. 0.8863 AE 0.665, p ¼ 0.0184; 0.2854 AE 0.1298 vs. 0.0128 AE 0.0158, p ¼ 0.0000, respectively), and the overexpression of Wnt1=b-catenin mRNA was aggressively associated with lymph node metastasis and advanced pathological stage ( p < 0.0001). The protein expression level of Wnt1= b-catenin was also significantly higher than that in the adjacent noncancerous tissues (0.3830 AE 0.0947 vs. 0.2721 AE 0.1474, p ¼ 0.0002; 0.2835 AE 0.0844 vs. 0.2352 AE 0.0670, p ¼ 0.0210, respectively); however, the overexpression was not associated with clinicopathologic characteristics. Meanwhile, the protein expression level of Wnt1 had no relevance with that of b-catenin. The overexpression of Wnt1=b-catenin might be an important molecular marker to predict the clinicopathologic stage and prognosis of ESCC, and the level of Wnt1=b-catenin mRNA was conversely correlated with lymph node metastasis and advanced pathological stage. The overexpression of Wnt1=b-catenin mRNA should also predict poor prognosis of ESCC; however, it might not be an independent prognostic factor.

Glypican 1 promotes proliferation and migration in esophagogastric adenocarcinoma via activating AKT/GSK/β-catenin pathway

“…Activated GPC1 then promotes interaction between FGF and PI3/AKT pathway, which is essential for cell survival by inhibiting apoptosis ( 45 ). GPC1 is also known to stimulate Wnt/β-catenin signaling ( 46 ) and there is also strong evidence of cooperation and synergy between PI3/AKT and Wnt/β-catenin driving certain gastrointestinal cancers ( 47 , 48 ). Our results are in accordance with these studies, as we noted an increased active p-AKT, p-GSK-β and p-β-catenin and increased accumulation of nuclear β-catenin in GPC1 overexpressed cells, whereas their levels were markedly reduced in GPC1 knockdown FLO1 cells.…”

Differential expression of canonical and non‐canonical Wnt ligands in ameloblastoma

“…Its protein localization and distribution patterns were comparable with those of previous reports (17, 20). Wnt‐1 overexpression has been reported in low‐grade subsets of cancers including well‐differentiated colorectal cancer (5), well‐differentiated oral squamous cell carcinoma (35), and well‐differentiated esophageal squamous cell carcinoma (36), as well as in KCOT (34) which has a similar local tumor growth behavior as the ameloblastoma. These findings (5, 34–36) and ours are of clinical significance because they indicate that Wnt‐1, which modulates cell–cell adhesion (3, 4), might represent an important marker of tumor progression and prognosis.…”

Inhibition of atypical protein kinase Cι induces apoptosis through autophagic degradation of β‐catenin in esophageal cancer cells

“…To investigate the oncogenic mechanism of PKCi in ESCC, we sought to identify the down-stream effectors of PKCi. b-catenin has been reported to be over-expressed in ESCC [21][22][23]. And it could be regulated by several important oncoprotein in ESCC cells [19,[24][25][26].…”