WNT3 (Wnt Family Member 3)

Moreover, CDNG-1 inhibited the Wnt/β-catenin pathway, evidenced by downregulated gene expression of Wnt3, LRP6 and β-catenin. Therefore, this study suggests that CDNG-1 exerts potential anti-proliferative, anti-migratory, and pro-apoptotic effects in liver cancer cells in a concentration-dependent manner, and hence, it could serve as a promising anticancer candidate for targeted therapies against liver cancer.

Circ_EPHB4 and YTHDF3 promote glioma progression by jointly targeting the Wnt3 signaling pathway, which may provide a new therapeutic strategy for gliomas.

None of the animals revealed the expected DGE pattern corresponding to a moderate to high H-ARS-severity degree. Hence, the Göttingen minipig did not qualify as another validation model for our specific gene set, which does not argue against their validity for other purposes.

Moreover, we found that WNT3/FZD7-mediated stemness properties of cancer cells were independent of the stemness-associated marker NANOG. In conclusion, we identified the FZD7(+)/CD133(+) signature as a potential prognosis marker and molecular therapeutic target, and we strengthened the hypothesis for the involvement of FZD7 in the enrichment of a cancer stem cell pool in HCC.

As the mechanism, FOXP3 induced CDH11 expression in fibroblasts, which augmented the Wnt3/β-catenin pathway, and blocking of CDH11 suppressed tumor invasion mediated by FOXP3(+) fibroblasts. Our results suggest that cancer cell-derived EVs regulate FOXP3 expression in stromal fibroblasts, attenuating antitumor immunity, and facilitating tumor invasion.

Cyclophosphamide (CTX), a cornerstone in breast cancer combination chemotherapy, frequently induces adverse effects including myelosuppression, gastrointestinal disturbances, hepatic impairment, and alopecia...MHJJ mitigates CTX-induced alopecia through epigenetic regulation of HFSCs, specifically via DNA hypomethylation-mediated activation of Wnt3/Wnt10a and suppression of Cer1/Axin1. This mechanism promotes follicular regeneration by restoring Wnt signaling homeostasis, positioning MHJJ as a promising adjuvant for chemotherapy-induced alopecia management.

Mechanistically, our studies revealed that the abnormal activation of the WNT canonical pathway promotes the recruitment of the transcription factor lymphoid enhancer-binding factor 1 (LEF1) to the ABCG2 promoter, thereby enhancing its transcriptional activity. In summary, our findings underscore the critical role of WNT3-mediated activation of the WNT canonical signaling pathway in upregulating ABCG2 expression, which enhances oxaliplatin efflux and contributes to the development of oxaliplatin resistance in OSCC.

Together, it was found that Wnt ligands Wnt3, Wnt3a, Wnt5b and Wnt7b are concomitantly upregulated in periodontitis and oral carcinogenesis. With these results, and the information retrieved from the literature, this review discusses the potential role of the Wnt/β-catenin pathway as a molecular mechanism that could interlink periodontitis and OSCC.

Circ_EPHB4 regulates Wnt3 expression through "sponge adsorption" of miR-424-5p, thereby modulating TMZ-resistant glioblastoma cell clonogenesis, apoptosis, and TMZ sensitivity, suggesting the potential of circ_EPHB4 as a therapeutic target for reversing drug resistance of gliomas.

This comprehensive review delineates Apoc1's mechanisms within malignant tumours and assesses its prognostic implications for patients with cancer. The aim is to shed light on potential novel therapeutic strategies in oncology, potentially revolutionising patient care and thereby enhancing patient survival rates and quality of life.

Tcf4 controls the balance between Paneth and goblet cells and is essential for antimicrobial peptide production in the small intestine. In colon adenomas, Paneth-like tumor cells drive antimicrobial gene expression and provide Wnt3 ligands, which may have implications for cancer therapy.

Pharmacological inhibition of Wnt/beta-Catenin signaling using FC101 significantly suppressed PCa growth, underscoring its potential as a therapeutic target. These findings reveal that Wnt/beta-Catenin signaling is active in NEPCa through multiple mechanisms and highlight the need for further investigation into the regulatory interplay between Wnt and YAP1 in prostate cancer.