ArticleJournal of gastrointestinal oncology2026
Overexpression of TAZ is associated with downregulation of E-cadherin and indicates poor prognosis in gastric cancer: a clinicopathological study.
Article in Journal of gastrointestinal oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Transcriptional co-activator with PDZ-binding motif (TAZ), a key downstream effector of the Hippo signaling pathway, regulates organ size and oncogenesis. However, its clinicopathological significance in gastric cancer (GC) and correlation with E-cadherin remain unclear. Thus, this study aimed to investigate these associations to evaluate TAZ as a prognostic biomarker and therapeutic target. Methods: TAZ messenger RNA (mRNA) and protein levels were assessed in fresh GC tissues and matched adjacent non-tumorous tissues using real-time quantitative polymerase chain reaction (qPCR) (8 pairs) and Western blotting (6 pairs). Additionally, TAZ and E-cadherin expression were evaluated in paraffin-embedded tissues from 98 GC patients and 25 normal controls via immunohistochemistry (IHC). Results: Compared to non-tumorous controls, TAZ mRNA (P=0.03) and protein levels were significantly upregulated in GC tissues. IHC analysis revealed a TAZ positivity rate of 67.3% in GC tissues, markedly higher than the 32.0% observed in normal gastric mucosa (P<0.001). TAZ overexpression was significantly associated with larger tumor diameter, lymph node metastasis, and advanced tumor-node-metastasis (TNM) stage (P<0.05). Notably, a significant negative correlation was identified between TAZ and E-cadherin expression (P=0.02). Kaplan-Meier survival analysis indicated that patients with TAZ-positive expression exhibited significantly shorter 5-year overall survival (P=0.002). Multivariate Cox regression analysis confirmed TAZ expression as an independent prognostic factor in GC patients. Conclusions: TAZ is overexpressed in GC and closely correlates with aggressive clinicopathological features and E-cadherin downregulation. TAZ may serve as a potential independent prognostic biomarker and therapeutic target in GC.
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