Overexpression of TAZ is associated with downregulation of E-cadherin and indicates poor prognosis in gastric cancer: a clinicopathological study

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.