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.
In order to further verify our conjecture that miR-361-5p mimic inhibited cell mobility through suppressing EMT via Wnt/β-catenin pathway in GC, the Wnt/β-catenin pathway activator LiCl was used in this study.
Chitinase 3-like 1-CD44 interaction promotes metastasis and epithelial-to-mesenchymal transition through β-catenin/Erk/Akt signaling in gastric cancer.
In addition, the downregulation of TP73-AS1 suppressed the expression of transcription factor 4 and β-catenin, which suggested that a decrease in TP73-AS1 suppressed the WNT/β-catenin signaling pathway in GC.
The results of a cDNA array revealed that protocadherin gamma subfamily A, 9 (PCDHGA9) was significantly decreased in SGC-7901 gastric cancer (GC) cells compared with GES-1 normal gastric cells and was strongly associated with the Wnt/β-catenin and transforming growth factor-β (TGF-β)/Smad2/3 signaling pathway.
In conclusion, TBL1XR1 contributes to GC tumorigenesis and progression through the activation of the β-catenin/MMP7/EGFR/ERK signalling pathway and may act as a new therapeutic target for GC.
Chi‑square tests suggested that STIM1 expression in GC tissues was significantly associated with E‑cadherin (P<0.001) and β‑catenin (P<0.001), whereas no association was observed between STIM1 and MMP‑9 expression (P>0.05).
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.
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.
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).
In conclusion, MALAT1 can promote tumorigenicity and metastasis in GC by facilitating VM and angiogenesis via the VE-cadherin/β-catenin complex and ERK/MMP and FAK/paxillin signaling pathways.
PS-1/γ-secretase cleaves E-cadherin and releases its bound protein partner, β-catenin, from the actin cytoskeleton, thereby allowing it to translocate into the nucleus and to activate the TCF/LEF-1 transcriptional activator, which may promote GC invasion and metastasis.In conclusion, PS-1 promotes invasion and metastasis in GC and may represent a novel prognostic biomarker and potential therapeutic target for GC treatment.