In summary, our study demonstrated that TXNDC12 could activate β-catenin via protein-protein interaction and promote ZEB1-mediated EMT and HCC metastasis.
Collectively, our data suggested that miR-623 suppressed the progression of HCC by regulating the PI3K/Akt, Wnt/β-catenin, and ERK/JNK pathways by targeting XRCC5 in HCC in vitro, indicating that miR-623 may be a target for the therapy of HCC.
Therefore, our study reveals the evolving nature of β-catenin in HCC to establish it as a compound tumor promoter during the progression of the disease.
The expression levels of CTNNB1 and MMP9 decreased by knocked down XRCC5 which may promote the progression of HCC via the Wnt/β-catenin signaling pathway.
PRRl1 mRNA expression was found positively correlated with β-catenin (R = 0.5472, P ˂ 0.0001), c-myc (R = 0.5527, P ˂ 0.0001) and cyclinD1 (R = 0.3948, P = 0.0003) in HCC tissues.
Some driver genes are significantly linked to HCC gender (<i>CTNNB1, ALB, TP53</i>, and <i>AXIN1</i>), race (<i>TP53</i> and <i>CDKN2A</i>), and age (<i>RB1</i>) disparities.
Clinicopathological parameters, progression-free survival (PFS) and overall survival (OS) were evaluated to analyze the association of β-catenin expression with prognosis for HCC patients after TACE.
We studied mice with activation of β-catenin in liver (Apc<sup>ko-liv</sup> mice) and male C57Bl/6 mice given injections of diethylnitrosamine, which each develop HCCs.
Finally, Western blot results indicated that silencing FBXO17 might function through downregulating the expression of proteins in wnt/β-catenin pathway such as c-Myc, MMP-9, and MMP-2 while upregulating GSK-3β level, thereby promoting the malignant progression of HCC.
A β‑catenin mutant and β‑catenin wild‑type HCC models were treated once daily with i) 10 mg/kg sorafenib, ii) 15 mg/kg refametinib (or 25 mg/kg selumetinib), or iii) sorafenib/refametinib.
Taken together, our results suggest that PAB exerts anti-cancer activity in HCC cells through inhibition of STAT3, ERK1/2, Akt, and GSK-3β/β-catenin carcinogenic signaling pathways, and may be used as a phytomedicine in the treatment of HCC.
In addition, immunohistochemistry (IHC) revealed that the amount of nuclear-localized β-catenin was significantly higher in KC/TFF1<sup>-/-</sup> mice than in KC mice and that human HCC tissue showed contradictory expression patterns for β-catenin and TFF1, confirming the in vitro observations.
ODC1 promotes proliferation and mobility via the AKT/GSK3β/β-catenin pathway and modulation of acidotic microenvironment in human hepatocellular carcinoma.
E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%).
In this study, we found that 34.8% of human HCC samples with FAK amplification also show β-catenin mutations, suggesting a co-occurrence of FAK overexpression and β-catenin mutations in HCC.
In hepatocellular carcinoma (HCC), Wnt/CTNNB1 mutations characterize the immune-excluded class (cold tumors) and might represent the biomarkers predicting resistance to immune checkpoint inhibitors.
We previously identified several genes that are regulated on the overexpression of β-catenin in the HCC cell line that are suggested to be novel Wnt/β-catenin targets playing effective roles in cancer.