Inhibition with ICG-001 significantly attenuated PY-induced fibrosis, confirming Wnt/β-catenin-dependent effects. These findings provide mechanistic insight into PY-induced renal injury and fibrosis.

Furthermore, the senolytic Src inhibitor dasatinib reduced senescence and fibrosis markers and attenuated β-catenin activity, suggesting that Src acts upstream of β-catenin in this context. Inhibition of β-catenin using ICG001 or PRI724 suppressed senescence and fibrosis markers and reduced downstream targets including CTGF and cyclin D1. These findings reveal a mechanistic link between mechanical stiffness, cellular senescence, and fibrosis in uterine fibroids, and identify Src and β-catenin as potential therapeutic targets.

KIF11 can promote the malignant phenotype and DDP resistance of tumor cells by activating the Wnt/β-catenin signaling pathway in OC. Therefore, KIF11 has the potential to serve as a biomarker for predicting OC progression and the efficacy of DDP treatment.

Mechanistically, PDRG1 activated Wnt/β-catenin signaling, elevating levels of β-catenin, c-Myc, and phosphorylated GSK-3β, and the oncogenic effects of PDRG1 were reversed by the Wnt pathway inhibitor XAV939...The pro-tumor effects of SP1 were rescued by PDRG1 silencing, indicating that SP1 acts through PDRG1. Collectively, our study identifies SP1 as an upstream transcriptional activator of PDRG1 and defines the SP1/PDRG1/Wnt/β-catenin axis as a key regulatory pathway promoting HCC progression, suggesting its potential as a prognostic biomarker and therapeutic target.

In vivo, the combination of L-asparaginase and doxorubicin, as well as treatment with XAV-939, significantly inhibited tumor growth, whereas NAC attenuated these effects. In conclusion, glutamine deprivation enhances doxorubicin sensitivity in osteosarcoma. Mechanistically, this chemosensitizing effect is mediated by downregulation of GLUD1, which promotes intracellular ROS accumulation and subsequently suppresses Wnt/β-catenin signaling.

Clinical analysis confirmed CBS overexpression correlates with OS progression. These findings highlight juglone's potential as a safe, effective anti-tumor agent targeting the CBS-Wnt/β-catenin pathway.

Compared to XAV939, LF3 more effectively inhibits nuclear β-catenin, might resulting in lower off-target toxicity and making it a favorable clinical candidate for targeting GBCs.

Targeting β-catenin interactions with co-activators p300/CBP using selective inhibitors (IQ-1 and ICG-001) effectively mitigated Wnt-driven ARSI resistance, restoring sensitivity to therapy in preclinical models...The identified Wnt signature holds potential as a biomarker for predicting and monitoring therapeutic outcomes. Concurrent targeting of AR and Wnt signaling represents a promising strategy to overcome treatment resistance, particularly in patients with Wnt-activating mutations.

Moreover, the Wnt/β-catenin inhibitor XAV939 reduced lactate production and H3K18la levels. Here, we demonstrate that the glycolysis/H3K18la/TK1/β-catenin positive feedback loop exacerbates dysfunction in OSCC initiation. These findings reveal a novel link between epigenetic regulation and lactate-driven metabolic reprogramming, which may lead to the development of innovative lactylation treatment approaches for OSCC therapy.

Following transfection, the Wnt signaling pathway inhibitor XAV-939 and agonist SKL2001 were administered to the KLF4-overexpressing cells...Results demonstrated that KLF4 overexpression inhibits EMT in gastric cancer cells through the Wnt/β-catenin signaling pathway. Thus, this study concludes that KLF4 may modulate EMT in gastric cancer cells via the Wnt/β-catenin pathway.

Combining Everolimus with the Wnt inhibitor XAV-939 slashed viability and invasion in resistant cells. Its loss defines a metastatic, therapy-resistant subtype targetable by dual mTOR/Wnt blockade. Therefore, MAGI3 expression may stratify patients for personalized therapy.

P3, N=276, Terminated, Biosplice Therapeutics, Inc. | Completed --> Terminated; Study OA-07 was designed to be conducted until the Sponsor closed it. Study OA-07 was administratively closed at Visit 6E (Week 100), with no safety concerns, one year into the open-label study as described in the protocol.