FZD10 (Frizzled Class Receptor 10)

Functional studies established that E2F2 directly regulates FZD10 expression, activating the Wnt/β-catenin pathway to sustain the stem-like state. Collectively, we unveil the E2F2/FZD10 axis as a previously unrecognized molecular conduit through which environmental arsenic reprograms mammary epithelial cells toward a BCSCs-like phenotype, providing mechanistic insight into arsenic-associated breast cancer risk and revealing a potential target for preventive intervention.

These clinically actionable genes, aberrantly expressed before treatment, may serve as early biomarkers for risk stratification. Further validation in PARPi-sensitive and -resistant ovarian cancer cohorts is needed.

No significant difference in body weight was observed between the groups during the observation period. FZD10 may be an appropriate target and 90Y-OTSA101 may have potential for the treatment of cervical cancer.

Unique mutational profiles were linked to a high proportion of Peruvians-from-Lima-like (1KG-PEL-like) genetic similarity. These findings highlight the need for targeted precision medicine approaches to address the distinct molecular characteristics of early-onset CRC in underrepresented populations.

Virtual screening of 1,094 FDA-approved drugs identified 17 potential inhibitors, with prazosin, rilpivirine, doxazosin, and nicergoline demonstrating significant cytotoxicity against NPC cells. Further molecular dynamics simulations and binding energy analyses confirmed the stable binding of these drugs to FZD10. The results suggest that these repurposed drugs could serve as promising candidates for targeted NPC therapy, warranting further investigation.

In this study, we verified the crucial role of hypoxia-inducible gene 2 (HIG-2) in lipid droplet (LD) accumulation and demonstrated that HIG-2 binding to frizzled class receptor 10 (FZD10) activated Wnt/β-catenin signaling pathway and increased its downstream insulin-like growth factor binding protein 2 (IGFBP2) level in microparticles (MPs) derived from glioma stem cells (GSCs), leading to decreased radiosensitivity and immunogenicity of MPs-receiving cells via the cross-talk between GSCs and non-stem glioma cells (GCs). These findings suggest that HIG-2 may be a promising target in glioma radiotherapy and/or immunotherapy.

Our study fills the gap of FMGs signature in predicting the prognosis of ESCC patients. These findings revealed that cluster subtypes and risk model of FMGs had effects on survival prediction, and were expected to be the potential promising targets for ESCC.

WMP significantly inhibits CAC tumorigenesis by up-regulating PPARα-mediated fatty acid oxidation, inhibiting the Wnt signaling pathway-mediated EMT, and suppressing CCL3/CCR1-mediated inflammatory responses.

In addition, drug sensitivity analysis identified 3 compounds, including BMS-754807, cytochalasin b, and linifanib, that could have a potential therapeutic effect on patients with the BLIS subtype. The risk prognosis model showed good prognostic value for the BLIS subtype patients, and the ten lncRNAs may be potential therapeutic targets.

The therapeutic and adverse effects were not significantly different between the three conjugates. Our findings indicate that among the three evaluated chelates, DOTAGA appears to be the most promising chelate to produce Ac-labeled OTSA101 with high binding affinity and high radiochemical yields while providing high absorbed doses to tumors and limited absorbed doses to bone marrow.

In addition, SOX9 could transcriptional inhibit DKK1 and activate FZD10 and MYC by binding to their promoters to affect the Wnt/β-catenin pathway. These results demonstrated SOX9 regulated the self-renewal and tumorigenicity of cervical cancer through Wnt/β-catenin pathway by directly transcriptional activation of FZD10, MYC and transcriptional inhibition of DKK1.

This data shows that lung cancer TME is significantly different from that of CRC. Only 20 immune biomarkers adequate to distinguish between the two TME. The relevant biomarkers included CD274 (PD-L1) as well as one marker for T-cells (CD8A) but three markers for B-cells (CD19, CD22 and CD79B).