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

Introduction

Background

Gastric cancer (GC) remains a major global health burden and is one of the leading causes of cancer-related mortality worldwide, particularly in East Asia. Despite substantial advances in surgical techniques, perioperative treatment, and multidisciplinary management, the prognosis of advanced GC remains unsatisfactory because many patients are diagnosed at a late stage and subsequently develop recurrence or metastasis (1-4). Therefore, identifying biologically meaningful molecular markers that can refine prognostic stratification and improve understanding of the mechanisms underlying tumor invasion and metastasis remains of substantial clinical importance.

Rationale and knowledge gap

The Hippo signaling pathway is an evolutionarily conserved growth-regulatory cascade that plays a central role in controlling organ size, tissue homeostasis, regeneration, and tumorigenesis (5-7). Transcriptional co-activator with PDZ-binding motif (TAZ, also known as WWTR1) is a major downstream effector of this pathway. When Hippo signaling is inactive, dephosphorylated TAZ accumulates in the nucleus and cooperates with TEA domain transcription factor (TEAD) and other transcription factors to activate transcriptional programs involved in cell proliferation, survival, stemness maintenance, and migration (5-8). Recent studies and reviews have further highlighted the pathogenic and therapeutic relevance of Hippo-Yes-associated protein (YAP)/TAZ dysregulation in GC (8). Aberrant TAZ expression has been documented in several solid tumors, including breast cancer, non-small cell lung cancer, and colorectal cancer (9,10). In GC, accumulating evidence also suggests that WWTR1/TAZ is involved in tumor progression and metastatic behavior, but its clinicopathological significance and prognostic value in a well-characterized patient cohort remain incompletely defined (8,11).

Epithelial-mesenchymal transition (EMT) is a crucial biological process that enhances tumor cell motility, invasiveness, and metastatic dissemination. Loss or downregulation of E-cadherin, a core component of epithelial adherens junctions, is one of the most recognized hallmarks of EMT and is generally associated with aggressive biological behavior and poor prognosis (12,13). Experimental studies have suggested that TAZ can participate in EMT-associated transcriptional reprogramming (14,15). However, clinicopathological evidence directly linking TAZ overexpression with E-cadherin downregulation in human GC tissues remains limited. Accordingly, evaluating TAZ together with E-cadherin may provide additional insight into the biological and prognostic heterogeneity of GC.

Objective

This study aimed to investigate TAZ expression in GC tissues and matched adjacent non-tumorous tissues, analyze its associations with clinicopathological characteristics and E-cadherin expression, and further evaluate the prognostic significance of TAZ overexpression in GC patients. Through this clinicopathological analysis, we sought to provide additional evidence supporting the value of TAZ as a prognostic biomarker and a potential therapeutic target in GC. We present this article in accordance with the REMARK reporting checklist (available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-1-0158/rc).

Methods

Subjects and ethics

This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the Ethics Committee of The First Affiliated Hospital of Sun Yat-sen University. Written informed consent was waived​ by the IRB due to the retrospective nature of the study and the use of de-identified, archival, formalin-fixed paraffin-embedded (FFPE) tissue specimens collected for clinical diagnostic purposes. Formalin-fixed, paraffin-embedded (FFPE) tissue specimens were retrospectively collected from 98 GC patients who underwent radical or palliative gastrectomy at our institution between January 2015 and February 2018. None of the patients had received preoperative radiotherapy or chemotherapy. Adjacent non-tumorous gastric mucosa (>5 cm from tumor margins) from 25 cases served as controls. Clinicopathological data, including age, sex, histological type, tumor diameter, tumor location, ascites, Borrmann classification, differentiation grade, depth of invasion, tumor-node-metastasis (TNM) stage, lymph node metastasis, distant metastasis, chemotherapy, and serum carcinoembryonic antigen (CEA) level, as well as postoperative follow-up information (up to December 31, 2025), were collected and entered into a database for subsequent clinicopathological correlation and survival analyses. Age was analyzed as a continuous variable. For categorical analyses, tumor diameter as <6.0 and ≥6.0 cm, and serum CEA level as <10 and ≥10 µg/L. Depth of invasion was classified as pT1–3 versus pT4. In cases in which older pathological records described invasion of the full thickness of the gastric wall without clearly specifying serosal penetration, and no adjacent organ invasion or peritoneal metastasis was documented, the surgical S stage was used for classification, with S0 defined as T3 and S1–S3 defined as T4a. Additionally, eight pairs of fresh GC tissues and matched adjacent normal mucosa were collected and snap-frozen in liquid nitrogen for subsequent messenger RNA (mRNA) and protein analyses.

RNA extraction and quantitative real-time polymerase chain reaction

Total RNA was extracted from eight pairs of fresh frozen tissues using TRIzol reagent (Qiagen) according to the manufacturer’s instructions. cDNA was synthesized using the M-MLV Reverse Transcriptase Kit (Invitrogen). Real-time quantitative polymerase chain reaction (qPCR) was performed on a Roche LightCycler 480 system using the SYBR Green PCR Kit (Fermentas). Primer sequences for TAZ were: forward 5'-TGTCATCTCAACCCCATCATCC-3', reverse 5'-CGCATCTCCACAGCCGACT-3'. GAPDH was used as the internal reference for relative normalization in this exploratory analysis of paired GC and adjacent non-tumorous tissues with primers: forward 5'-AGCCACATCGCTCAGACAC-3', reverse 5'-GCCCAATACGACCAAATCC-3'. Relative expression levels were calculated using the 2^−ΔΔCt method.

Western blotting

Protein lysates were extracted from six pairs of fresh tissues, quantified via BCA assay, separated by SDS-PAGE, and transferred to PVDF membranes. Membranes were blocked with 5% non-fat milk and incubated overnight at 4 ℃ with mouse anti-human TAZ monoclonal antibody (1:300, Abcam, ab118373) and mouse anti-GAPDH antibody (1:10,000, Earthox). Following washes, membranes were incubated with HRP-conjugated secondary antibodies, and signals were detected using an ECL chemiluminescence system (Kodak).

Immunohistochemistry

Immunohistochemical staining was performed on 4-µm serial sections from 98 GC and 25 control tissues using the EnVision two-step method. Sections were deparaffinized, rehydrated, and subjected to antigen retrieval in 0.01 M citrate buffer (pH 6.0) via high-pressure heating. Endogenous peroxidase activity was blocked, followed by incubation with mouse anti-human TAZ monoclonal antibody (1:300, Abcam) or mouse anti-human E-cadherin monoclonal antibody (Abcam) at 37 ℃ for 1 hour. Detection was achieved using a universal secondary antibody kit (Dako, GK500705) and DAB chromogen, with hematoxylin counterstaining.

Evaluation of immunohistochemical staining

Two senior pathologists independently evaluated immunohistochemical results in a blinded manner. Scoring incorporated staining intensity (0: none; 1: light yellow; 2: brown-yellow; 3: dark brown) and percentage of positive cells (0: ≤5%; 1: 6–25%; 2: 26–50%; 3: 51–75%; 4: ≥76%). The immunoreactive score (IRS) was calculated as the product (range, 0–12). Expression levels were categorized as: negative (0), weak positive [1–2], moderate positive [3–6], and strong positive [≥8]. For statistical analysis, moderate and strong positive were defined as high expression, while negative and weak positive were classified as low/negative expression.

Statistical analysis

Data analysis was conducted using SPSS 31.0 software. Paired t-tests were employed for continuous variables. Chi-square tests were used for categorical data and clinicopathological correlations. Survival curves were generated using the Kaplan-Meier method, and differences were assessed using the log-rank test. Univariate and multivariate survival analyses were performed using Cox proportional hazards regression models. P<0.05 was considered statistically significant.

Results

TAZ mRNA and protein levels were significantly upregulated in GC tissues

TAZ mRNA relative expression levels were quantified in eight pairs of fresh GC and matched adjacent non-tumorous tissues using qPCR. Results indicated significantly higher TAZ mRNA levels in GC tissues compared to controls (P=0.03), suggesting transcriptional upregulation (Figure 1).

Figure 1 Relative TAZ mRNA expression in eight paired gastric cancer tissues and matched adjacent non-neoplastic mucosa. Relative TAZ mRNA expression was determined by quantitative real-time polymerase chain reaction and calculated using the 2^−ΔΔCt method. Each dot represents one sample, and matched samples are connected by lines. N, adjacent non-neoplastic mucosa; T, tumor tissue; TAZ, transcriptional co-activator with PDZ-binding motif.

To confirm changes at the protein level, Western blot analysis revealed markedly elevated TAZ protein (44 kDa) expression in GC tissues compared with adjacent non-tumorous tissues in six matched pairs (Figure 2).

Figure 2 TAZ protein expression in six paired samples. N, adjacent non-neoplastic mucosa; T, tumor tissue; TAZ, transcriptional co-activator with PDZ-binding motif.

Immunohistochemical analysis: TAZ expression characteristics and associations with clinicopathological parameters

Immunohistochemical staining was performed on 98 GC tissues and 25 normal gastric mucosa samples. Representative TAZ immunostaining patterns in GC tissues with different differentiation status and in non-neoplastic gastric mucosa are shown in Figure 3A-3F. TAZ staining was predominantly cytoplasmic, with nuclear localization observed in some cases. The TAZ positivity rate in GC tissues was 67.3% (66/98), significantly higher than in normal gastric mucosa (32.0%, 8/25; P<0.001).

Figure 3 Representative immunohistochemical staining patterns of TAZ in gastric cancer and non-neoplastic gastric mucosa. (A) Positive TAZ expression in well-differentiated adenocarcinoma, with staining predominantly localized to the cytoplasm and scattered nuclear positivity (arrows). (B) Negative TAZ expression in well-differentiated adenocarcinoma. (C) Positive TAZ expression in poorly differentiated adenocarcinoma, with staining predominantly localized to the cytoplasm and scattered nuclear positivity (arrows). (D) Negative TAZ expression in moderately to poorly differentiated adenocarcinoma. (E) Positive TAZ expression in non-neoplastic mucosa, mainly localized to the cytoplasm. (F) Negative TAZ expression in non-neoplastic mucosa. EnVision two-step immunohistochemistry, ×400. TAZ, transcriptional co-activator with PDZ-binding motif.

Clinicopathological analysis demonstrated significant positive correlations between TAZ overexpression and tumor diameter (≥6.0 cm, P=0.046), lymph node metastasis (P=0.006), and advanced TNM stage (III–IV, P=0.03) (Table 1). However, no significant associations were found with patient age, sex, tumor location, differentiation grade, Borrmann classification, or CEA levels (P>0.05).

Negative correlation between TAZ and E-cadherin expression

Immunohistochemical results showed an E-cadherin positivity rate of 50.0% (49/98) in GC tissues, primarily localized to the cell membrane. Statistical analysis revealed a significant negative correlation between TAZ and E-cadherin expression in GC tissues (P=0.02). Furthermore, low E-cadherin expression was closely associated with poor differentiation (P=0.03), invasion depth (P=0.02), lymph node metastasis (P=0.02), and advanced TNM stage (P=0.03). Representative E-cadherin immunostaining patterns in GC tissues and normal gastric mucosa are shown in Figure 4A-4D.

Figure 4 Representative immunohistochemical staining patterns of E-cadherin in gastric cancer and normal gastric mucosa. (A) Positive E-cadherin expression in poorly differentiated adenocarcinoma, observed in a subset of tumor cells and localized to the cell membrane. (B) Negative E-cadherin expression in poorly differentiated adenocarcinoma. (C) Positive E-cadherin expression in well-differentiated adenocarcinoma, observed in the majority of tumor cells and localized to the cell membrane. (D) Positive E-cadherin expression in normal mucosa, strongly observed in nearly all epithelial cells and localized to the cell membrane. EnVision two-step immunohistochemistry, ×400. TAZ, transcriptional co-activator with PDZ-binding motif.

Survival analysis: TAZ as an independent prognostic factor in GC

Kaplan-Meier survival analysis demonstrated that the 5-year overall survival rate for TAZ-positive patients (32.6%) was significantly lower than for TAZ-negative patients (69.3%; log-rank P=0.002, Figure 5).

Figure 5 Postoperative Kaplan-Meier survival curves for gastric cancer patients stratified by different TAZ expression levels. TAZ, transcriptional co-activator with PDZ-binding motif.

Similarly, E-cadherin-positive patients exhibited significantly better survival than E-cadherin-negative patients (P=0.02; Figure 6).

Figure 6 Postoperative Kaplan-Meier survival curves for gastric cancer patients stratified by different E-cadherin expression levels.

Combined analysis further indicated that patients with TAZ-positive and E-cadherin-negative expression (TAZ+/E-cadherin−) had the poorest prognosis, with a 5-year survival rate of 24.1%, significantly lower than other subgroups (P=0.004, Figure 7).

Figure 7 Postoperative Kaplan-Meier survival curves for gastric cancer patients stratified by combined TAZ and E-cadherin expression. TAZ, transcriptional co-activator with PDZ-binding motif.

Univariate Cox proportional hazards regression identified tumor diameter, Borrmann classification, invasion depth, lymph node metastasis, distant metastasis, E-cadherin, and TAZ expression as significantly associated with overall survival. Multivariate analysis confirmed TAZ overexpression (HR =2.505, 95% CI: 1.143–5.490, P=0.02), along with invasion depth, lymph node metastasis, distant metastasis, and Borrmann classification, as independent risk factors for GC prognosis (Table 2).

Discussion

GC, a prevalent gastrointestinal malignancy worldwide, is primarily associated with poor patient prognosis due to its insidious onset and high invasiveness. Despite advances in standard treatments, such as surgical resection combined with perioperative chemoradiotherapy, which have extended survival to some extent, recurrence and metastasis rates remain high in advanced-stage GC (1-4). Thus, elucidating the key molecular networks driving GC invasion and metastasis and identifying precise biomarkers for high-risk prognostic stratification represents a critical challenge in current translational research. This study focuses on TAZ (WWTR1), an effector of the Hippo signaling pathway, through large-scale retrospective analysis of clinical samples. Abnormal TAZ activation patterns in GC were revealed, along with a negative correlation with the EMT key molecule E-cadherin, offering novel insights into GC progression mechanisms.

TAZ mRNA and protein expression levels were first confirmed to be significantly elevated in GC tissues compared to adjacent normal tissues, with the protein predominantly localized in the nucleus or cytoplasm. This finding aligns with TAZ’s role as a transcriptional co-activator. Under physiological conditions, Hippo pathway activation promotes LATS1/2-mediated phosphorylation of TAZ, resulting in cytoplasmic sequestration and proteasomal degradation. In contrast, when Hippo signaling is impaired, TAZ translocates into the nucleus and drives transcriptional programs favoring proliferation, survival, stemness, and migration (5-8). Recent reviews have emphasized that aberrant Hippo-YAP/TAZ signaling is increasingly recognized as an important contributor to GC pathogenesis and a potential therapeutic vulnerability (8). In addition, recent mechanistic work has shown that upstream oncogenic regulators can promote gastric adenocarcinoma progression through activation of Hippo/YAP1 signaling, further supporting the relevance of this pathway in gastric tumor biology (16). In the present cohort, the association between high TAZ expression and larger tumor size, nodal metastasis, and advanced stage is therefore consistent with the concept that TAZ contributes to a more aggressive tumor phenotype.

In-depth analysis of clinicopathological features revealed a highly significant positive correlation between high TAZ expression and larger tumor diameter (≥6.0 cm), positive lymph node metastasis, and advanced TNM stage (III–IV) (P<0.05). Robust molecular biology mechanisms underpin this association. Regarding tumor growth, nuclear-localized TAZ binds to the TEAD transcription factor family, initiating transcription of downstream targets such as CTGF, CYR61, and AXL. These genes not only directly promote G1/S cell cycle progression but also facilitate tumor angiogenesis through paracrine signaling, supporting rapid tumor expansion (14). TAZ has been implicated in metastatic progression and stemness-related programs in several malignancies, and WWTR1/TAZ has been reported as a metastatic biomarker in gastric cardia adenocarcinoma (11). This stemness enhances anti-apoptotic capabilities, enabling survival under lymphatic shear stress (anoikis resistance), and promotes distant organ colonization and the formation of metastatic foci. Clinical data from this study corroborate this mechanism: tumors with high TAZ expression exhibit greater invasiveness and earlier regional lymph node involvement. This suggests that for early GC patients with biopsy-confirmed high TAZ expression, clinicians may consider more extensive D2 lymph node dissection or more aggressive adjuvant therapy regimens postoperatively.

Furthermore, a significant negative correlation between TAZ and E-cadherin expression (P=0.02) was identified, providing key clues to the pathways through which TAZ promotes GC metastasis. E-cadherin, a core component of adherens junctions in epithelial cells, exhibits loss of membrane expression as a hallmark of EMT initiation—the pivotal step enabling tumor invasiveness (12). Recent clinical evidence continues to support the importance of E-cadherin-deficient biology in GC (8). Our histological evidence supports the “Hippo-EMT interplay” hypothesis. On the one hand, TAZ acts as a potent EMT inducer by forming complexes with transcription factors ZEB1/2 or Snail/Slug, directly binding to the CDH1 (E-cadherin-encoding gene) promoter to repress E-cadherin transcription. This disrupts intercellular adhesions, driving mesenchymal-like changes and enhanced motility (15). On the other hand, E-cadherin itself serves as an upstream regulator of the Hippo pathway. Prior cell biology studies show that intact cell-cell contacts (via E-cadherin) recruit Hippo pathway components to the membrane, activating LATS kinases to inhibit TAZ. In GC tissues where E-cadherin is lost, this contact inhibition signal is abrogated, further promoting TAZ nuclear activation. Thus, a malignant “positive feedback loop” is hypothesized in GC progression: TAZ upregulation suppresses E-cadherin, while E-cadherin loss reciprocally enhances TAZ activation. This dual mechanism collectively drives epithelial-to-mesenchymal phenotypic shifts in GC cells, culminating in peritoneal dissemination and distant metastases.

Survival analysis outcomes underscore the clinical translational value of this molecular mechanism. Both univariate and multivariate Cox regression analyses confirmed TAZ as a potent prognostic factor independent of TNM stage (HR =2.505, P=0.02). This implies that, even among patients at the same TNM stage, those with high TAZ expression experience significantly shorter survival. This conclusion aligns with findings by Wang et al. (17) in colorectal cancer and Xie et al. (10) in non-small cell lung cancer, indicating TAZ may serve as a pan-cancer poor prognostic marker. Of greater clinical relevance are the combined survival analysis results: the subgroup exhibiting “high TAZ expression” and “low E-cadherin expression” displayed the worst prognosis, with a 5-year survival rate of only 24.1%. This subgroup likely represents a refractory GC subtype characterized by “high EMT phenotype” and “elevated stemness”. For these patients, conventional cytotoxic chemotherapy may yield limited efficacy, as EMT states often confer resistance to 5-fluorouracil and platinum-based agents. This highlights the potential in future clinical practice to employ TAZ and E-cadherin as combined molecular probes to identify this high-risk subgroup and to explore whether targeted Hippo pathway interventions—such as verteporfin to disrupt YAP/TAZ-TEAD interactions—could confer survival benefits (18).

Certain limitations of this study warrant addressing in future work. As a single-center retrospective study with a relatively small sample size (n=98), selection bias may be present; multi-center, large-scale prospective cohorts are needed to validate TAZ prognostic cut-off values. In addition, GAPDH was used as the single internal reference gene for qPCR normalization in this exploratory paired-tissue analysis. Although the paired design helped reduce inter-sample variability, the use of a single housekeeping gene may still introduce normalization bias. Notably, the observed upregulation of TAZ was further corroborated by Western blotting and immunohistochemical, which strengthened the overall consistency of the findings. Future studies should validate reference gene stability and ideally include multiple housekeeping genes to improve the robustness of qPCR-based expression analysis. Additionally, while a negative correlation between TAZ and E-cadherin was observed, direct molecular interactions in GC tissues were not verified via co-immunoprecipitation (Co-IP) or chromatin immunoprecipitation (ChIP). Finally, with the emergence of immunotherapy in GC, exploring whether TAZ modulates the tumor immune microenvironment through PD-L1 regulation represents a promising avenue.

In summary, this study not only confirms TAZ overexpression in GC and its independent prognostic value but, more importantly, elucidates its close associations with E-cadherin downregulation and the EMT process through clinicopathological data. These findings support a molecular model wherein TAZ promotes GC invasion and metastasis by inducing EMT and sustaining tumor stemness. In the era of precision medicine, TAZ emerges as a novel biomarker for GC prognostic assessment and provides a theoretical foundation for overcoming chemotherapy resistance and developing targeted therapies.

Conclusions

In conclusion, TAZ overexpression was confirmed in GC tissues and correlated closely with aggressive clinicopathological features, including lymph node metastasis and advanced TNM stage. A significant negative correlation was observed between TAZ overexpression and E-cadherin downregulation, suggesting that TAZ is involved in EMT-driven GC progression. Critically, TAZ serves as an independent prognostic factor for postoperative survival in GC patients. Assessing TAZ expression, particularly in combination with E-cadherin, helps identify high-risk patients and offers potential new targets for targeted GC therapy.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the REMARK reporting checklist. Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-1-0158/rc

Data Sharing Statement: Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-1-0158/dss

Peer Review File: Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-1-0158/prf

Funding: The study was supported by Guangxi Medical and Health Appropriate Technology Development and Promotion Project (No. S2025029).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-1-0158/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the Ethics Committee of The First Affiliated Hospital of Sun Yat-sen University. Written informed consent was waived​ by the IRB due to the retrospective nature of the study and the use of de-identified, archival, formalin-fixed paraffin-embedded (FFPE) tissue specimens collected for clinical diagnostic purposes.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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