Mechanistically, PHF8 interacts with β-catenin, and binds to the promoter region of vimentin, leading to the promotion of vimentin transcription.In addition, we show that <i>H. pylori</i>, the single most important risk factor for GC, markedly induce PHF8 expression.Our results suggest that <i>H. pylori</i>-induced PHF8-β-catenin-vimentin axis activation is a novel mechanism for GC malignant progression.
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.
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.
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.
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.
Overexpression of miR-302b impaired GC cell migratory and invasive properties robustly and suppressed cell proliferation by arresting cells at G0-G1 phase in vitro. miR-302b exhibited anti-tumor activity by reversing EphA2 regulation, which relayed a signaling transduction cascade that attenuated the functions of N-cadherin, β-catenin, and Snail (markers of Wnt/β-catenin and epithelial-mesenchymal transition, EMT).
These data suggest that inactivating mutations of the Siah-1 may contribute to the development of gastric cancer through beta-catenin stabilization and apoptosis block.