In addition, the immunohistochemical expression pattern of beta-catenin in 303 consecutive gastric cancers was determined and their relationships with clinicopathologic features and patient outcome were investigated.
Collectively, knockdown of AGGF1 inhibits the invasion and migration of gastric cancer via epithelial-mesenchymal transition through Wnt/β-catenin pathway.
Ncleotides activated P2Y6 receptors to raise cytosolic Ca<sup>2+</sup> concentrations in GC cells through store-operated calcium entry (SOCE), and then mediated Ca<sup>2+</sup>-dependent inhibition of β-catenin and proliferation, eventually leading to GC suppression.
Furthermore, knockdown of UBE2C using siRNA markedly reduced the level of phosphorylation AURKA (p‑AURKA) via Wnt/β‑catenin and PI3K/Akt signaling pathways suppressed the occurrence and development of gastric cancer.
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.
The high expression of marginal KPNA2 was significantly associated with β-catenin accumulation in the nucleus and poor prognosis in two independent GC cohorts (discovery cohort, n = 90, P = 0.018; validation cohort, n = 89, P = 0.0125).
The present findings indicate that DAP3 deficiency-induced chemoresistance in gastric cancer is at least partially mediated through the β-catenin/LGR5/Bcl-2 axis.
We detected seven somatic mutations in a portion of exon 3 encoding for the glycogen synthase kinase 3beta phosphorylation consensus region of the beta-catenin gene in 43 gastric cancers.
Furthermore, the overexpression of Egr-1 upregulated β-catenin expression level, promoted cell proliferation, increased cell population in S-phase and enhanced gastric cancer cell migration and invasion in vitro.
Silencing of CUL4B also resulted in decreased Wnt and β‑catenin expression, but increased expression of GSK‑3β, caspase‑3 and cyclin E. These results indirectly demonstrate that CUL4B enhances the proliferation and invasion abilities of gastric cancer cells by upregulating the constituent factors Wnt and β‑catenin, as well as by negatively regulating the mRNA and protein expression of GSK‑3β, caspase‑3 and cyclin E. The potential mechanism of CUL4B highlighted in the present study may be helpful for the treatment of patients with gastric cancer.
Thus, this review centers on the strong associations between Wnt/β-catenin pathway and microRNAs during alteration of EMT in GC, which may induce advantageous therapeutic strategies for human gastric cancer.
These findings suggest that the expression of WISP2 and β-catenin might be a favorable biomarker for prediction and prognosis in the early stage of GC.
A small portion of GCs expressed LGR5.Although LGR5 was associated with poor survival in GCs with nuclear β-catenin, LGR5 expression in GC cells had no effects on the growth and migration, requiring a further study exploring a biological role of LGR5 in GCs.
Although, Siah1 could not increase degradation of the cytosolic β-catenin and its nuclear translocation, it enhanced degradation of the membrane-bound β-catenin in the infected GCCs.
In addition, we showed that upregulation of HEF1 increased Wnt5a expression and the nuclear translocation of β-catenin, thereby resulting in poor differentiation in GC.