Mechanically, TIPE1 directly targets β-catenin and promotes β-catenin degradation in a protease-dependent manner, and Wnt/β-catenin signaling plays a crucial role during TIPE1-mediated stemness inhibition in colon cancer.
The expression of β-catenin and STT3A/B in colon cancer tissues was initially detected by immunohistochemistry, followed by correlation analyses of the survival rate with the expression of β-catenin and STT3A/B as well as identification of the interaction between β-catenin and STT3A/B.
The selective ERα antagonist could significantly decrease Wnt2b/LRP8/Dvl1 expression, increase destruction complex (Axin2/GSK3a/APC) expression, and promote degradation of β-catenin in colon carcinoma cell by inhibited NLRP3 expression.
In conclusion, targeting CBP/β-catenin, combined with PD-1/PD-L1 immune checkpoint blockade, shows potential as a new therapeutic strategy for treating liver metastasis during colon cancer.
In addition, PIK3CD expression in colon cancer tissues positively correlated with β-catenin abnormal expression, which was an independent predictor for OS of colon cancer patients.
<i>Conclusion</i>: ZEB2-AS1 could promote colon cancer cell proliferation and inhibit apoptosis to promote the progression of colon cancer by upregulating the expression of β-catenin protein.
In this study, we synthesized Dicer-substrate siRNA conjugated with palmitic acid at the 5'-end of the sense strand (C16-DsiRNA), and examined its RNAi effect on β-catenin as a target gene in a colon cancer cell line, HT29Luc, both in vitro and in vivo.
By an in silico study, we present here a possible mechanism of interaction between the sesame lignans and β-catenin leading to inhibition of formation of the said complex, thereby elevating some of these ligands as potential lead molecules in the development of drugs for treatment of colon cancer.
Colon cancer cells secrete and express high levels of β-catenin, which may stimulate autocrine signaling and further enhance activities of the canonical Wnt signaling pathway.
MiR-155 directly regulates β-catenin at the transcriptional level, and promotes the invasion potential of colon cancer cell, at least partly through the upregulation of β-catenin.
Overall, the current study has identified activation of the Wnt/β-catenin pathway as a novel fundamental cause of colon cancer resistance to BRAF inhibition.
Our results establish MACC1 as a transcriptional target of Wnt/β-catenin signaling and suggest that DBC1 plays a key role in colorectal cancer progression through Wnt/β-catenin-MACC1 signaling axis.