The aberrant nucleocytoplasmic shuttling of active PTK6/β-catenin is reversed by expressing the PSPC1 C-terminal interacting domain (PSPC1-CT131), thereby suppressing PSPC1/PTK6/β-catenin-activated metastasis to prolong the survival of HCC orthotopic mice.
Molecular changes in HCC collectively contribute to Wnt/β-catenin, as a tumor proliferative signaling pathway, toll-like receptors (TLRs), nuclear factor-kappa B (NF-κB), as well as the c-Jun NH2-terminal kinase (JNK), predominant signaling pathways linked to the release of tumor-promoting cytokines.
E-cadherin signaling plays an important role in hepatocellular carcinoma (HCC) initiation and progression considering the highly mutated frequency of CTNNB1 (27%).
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.
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.
Our studies indicate that MEISC/D promote HCC development via Wnt/β-catenin and Hippo/YAP signaling pathways, highlighting the complex molecular network of MEIS2C/D in HCC pathogenesis.
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.
In summary, our study demonstrated that TXNDC12 could activate β-catenin via protein-protein interaction and promote ZEB1-mediated EMT and HCC metastasis.
The development of HCC involves deregulation in several cellular signalling pathways including Wnt/FZD/β-catenin, PI3K/Akt/mTOR, IRS1/IGF, and Ras/Raf/MAPK.
ODC1 promotes proliferation and mobility via the AKT/GSK3β/β-catenin pathway and modulation of acidotic microenvironment in human hepatocellular carcinoma.
Among this molecular subgroup, CTNNB1-mutated HCCs constitute a homogeneous subtype, exhibiting cholestasis and microtrabecular and pseudoglandular architectural patterns.
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.
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.