Additionally, the in vivo regulatory effects of β-catenin silencing and KYA1797K were evaluated by assessing tumor formation, detecting CD8 and GZMB expression and CD8<sup>+</sup> T cell viability.
In addition, we found a significant decrease in the growth and weight of tumors and an increase in tumor cell apoptosis in TRIM58-overexpression nude mice, which were also accompanied by reduced β-catenin expression.<b>Conclusions</b>: These data suggest that TRIM58 may function as a tumor suppressor in GC and potentially suppress the tumor growth of gastric cancer by inactivation of β-catenin signaling via ubiquitination.
For cases with available tumor tissue (n = 86), subgroups were assigned by either 450 K methylation array or immunohistochemistry and CTNNB1 sequencing.
However, we did not identify any mutations in 54 oncogenes and tumor suppressor genes (including CTNNB1) by next-generation sequencing analysis, and PCR Sanger sequencing did not reveal FOXL2 C134W mutation, suggesting the possibility of heterogenous pathogenesis of these tumors.
We evaluated epithelial-mesenchymal phenotypic characteristics across a range of tumor histologies using a validated, high resolution digital microscopic immunofluorescence assay (IFA) that incorporates β-catenin detection and cellular morphology to delineate carcinoma cells from stromal fibroblasts and that quantitates the individual and co-localized expression of the epithelial marker E-cadherin (E) and the mesenchymal marker vimentin (V) at subcellular resolution ("EMT IFA").
Recurrence rate in patients with stage IA disease at diagnosis was significantly higher in patients whose tumors were CTNNB1 mutated compared with CTNNB1 wild-type (30% vs. 0%; P=0.025) and included distant metastases; all recurrent tumors in this group harbored exon 3 mutations and were histologically low grade (5 grade 1, 2 grade 2).
Fibulin-2 and β-catenin had a negative correlation (r=-0.361, P=0.003), but was closely correlated with the tumor size and lymph node metastasis (P<0.05).
The Wnt/β-catenin pathway is a crucial oncogenic signal in relation to tumor immune evasion; however, none of the Wnt inhibitor under clinical or preclinical phases has demonstrated satisfactory specificity.
Our present study provided a novel mechanism involved in the inflammation-driven cancer progression through tumor immune escape and downstream gene regulation of WNT/β-catenin pathway-dependent manner.
HER2 expression pattern is linked with tumor stage and overall survival; the transforming function of HER2 is found more relevant through β-catenin and SMAD3.
Furthermore, PLK4 knockdown inactivated the Wnt/β‑catenin pathway in CRC cells in vitro and in vivo, and suppressed the growth of xenograft tumors in nude mice.
Curcumin administration participates to the downregulation of the WNT/β-catenin pathway and thus, through this action, in tumor growth control.Curcumin act as PPARγ agonists.
Additionally, the levels of estrogen receptor and progesterone receptor were decreased, whereas human epidermal growth factor receptor 2 and β-catenin were upregulated in the Kindlin-2-induced mammary tumors.
Direct binding of TTPAL with TRIP6 in the cytoplasm inhibited ubiquitin-mediated degradation of TRIP6 and, subsequently, increased levels of TRIP6 displaced β-catenin from the tumor suppressor MAGI1 via competitive binding.
Since the APC product interacts with beta-catenin, APC variants may, in addition to CTNNB1, contribute to the pathogenesis of solid pseudopapillary neoplasms via the Wnt signaling pathway.
Furthermore, we observed a significant correlation of β-Catenin overexpression with higher tumor stage pT3c (ρ = 0.230, p = 0.028) and initial lymph node metastases (ρ = 0.236, p = 0.025).
Analyses of tumors with various NF-1 expression patterns (c+/n-; c-/n+ combined with c+/n+, and c-/n-) revealed that aberrant nuclear accumulation of NF-1 is accompanied by nuclear accumulation of beta-catenin, suggesting that they may act synergistically to define the tumor's biology.