WNT7B (Wnt Family Member 7B)

Animal study revealed that knockdown of exosomal METTL14 from AML-MSC reduced AML tumorigenesis by decreasing HOXA3 and WNT7B expression. AML-MSC-derived exosomal METTL14 facilitated AML cell growth and glycolysis by activating the HOXA3/WNT7B axis, providing a new mechanism for understanding AML-MSC-derived exosomes to promote AML progression.

Collectively, our findings uncover that METTL3-mediated m6A modification of CACNA1E contributes to OS progression and chemoresistance through enhancing WNT7B-mediated non-canonical Wnt/Ca2+ signaling. Targeted inhibition of CACNA1E in combination with MTX may be a promising alternative therapeutic strategy for patients with MTX-resistant OS.

Inhaled BEAT outperforms linked dual antibody targeting PD-L1 and Wnt7b in vivo. This approach to tandem protein display may be applicable to diverse ICI-resistant cancers.

Understanding the GPR124‑Wnt‑PPARγ axis provides novel therapeutic opportunities for combination targeting strategies in chronic inflammatory conditions, where the balance between pro‑angiogenic Wnt activation and anti‑inflammatory PPARγ signaling determines disease outcomes. The present review examines the molecular architecture of GPR124‑PPARγ crosstalk, analyzes pathophysiological implications across multiple organ systems, and evaluates emerging therapeutic strategies for targeting this regulatory network in chronic inflammatory diseases.

The mice were assigned to 6 groups, including the normal group, the model (CIA) group, the model + CSJBD-L (8.1 g/kg) group, the model + CSJBD-M (16.2 g/kg) group, the model + CSJBD-H (32.4 g/kg) group, and the model + leflunomide (LEF) (0.05 mg/10 g) group, with 10 mice in each group...Wnt7b overexpression reversed the inhibitory effect of CSJBD on the Wnt/β-catenin signaling pathway and the proliferation of RA FLSs, indicating that Wnt7b is the direct target of CSJBD. CSJBD inhibits RA pathology by blocking the WTAP-Wnt7b-Wnt/β-catenin signaling axis, with Wnt7b identified as a direct therapeutic target of CSJBD.

Gastric tumors can bypass niche dependence by acquiring KRAS-MAPK-SMAD2/3-driven epithelial WNT secretion. Targeting this axis-through MAPK inhibition, SMAD2/3 blockade, or suppression of WNT secretion-may represent a therapeutic vulnerability in gastric cancer and other KRAS-high malignancies.

Adding a 59-patient four-year-prognosis cohort allowed us to rigorously assess the clinical relevance of these methylation change trends. These shallow changes reflect tumor characteristics and have the potential for prognostic prediction in patients, warranting further investigation.

Our study reveals a novel regulatory axis in which H2BC9 K44 lactylation activates Wnt7b transcription and downstream Wnt/β-catenin signaling, driving ESCC progression. Targeting H2BC9 lactylation may offer a promising therapeutic strategy to overcome tumor growth and immune evasion in ESCC.

Furthermore, co-expression and drug sensitivity analyses revealed that WNTs influence the efficacy of multiple anti-cancer agents, offering potential targets for precision oncology. This study provides novel insights into the multifaceted role of WNT genes in BRCA, identifying them as promising prognostic indicators and immunotherapeutic targets that warrant further clinical exploration.

In addition, ZNF831 inhibited tumour growth and progression through YTHDF1 mediated translational regulation of WNT pathway key genes WNT7B and FZD5. These results demonstrated that the feedback loop of ZNF831-YTHDF1-DNMT1/3a regulates cell growth, migration and invasion via WNT7B-FZD5-β-catenin axis, further providing a new idea for targeting epigenetic regulators of LC.

Treatment combining a porcupine inhibitor WNT974 with αPD1 reprogrammed the immune suppressive tumor microenvironment (TME) to bolster antitumor immune responses and extended the survival of mice bearing orthotopic GBM, with 25% long-term survivors...Conversely, an increase in monocytic MDSCs and phosphorylation of pro-oncogenic proteins was associated with resistance to the combination therapy. Collectively, our preclinical findings provide a strong rationale to test Wnt7b/β-catenin inhibition with αPD1 therapy in GBM patients with elevated Wnt7b/β-catenin signaling.

In conclusion, ZEB1 positively regulates Wnt/β-catenin signaling in lung cancer and contributes to cancer progression. ZEB1 knockdown increases the efficacy of Docetaxel in lung cancer.