Moreover, the enhanced 1O2 production facilitates sonodynamic therapy (SDT), effectively abating tumors. This nanoprobe not only improves imaging accuracy but also provides real-time monitoring of therapeutic efficacy, offering a promising approach for personalized cancer treatment and advancement of precision theranostics.
Congruently, tumor spheroids formed from MDA-MB-231 cells that were pretreated with low-density FZD7-NS had significantly reduced area, metabolic activity, and cell number compared to those treated with high-density FZD7-NS. These results emphasize the importance of determining the appropriate surface ligand density when designing antibody-nanoparticle conjugates for therapeutic utility.
Mechanistically, USP30-AS1 acts as a competing endogenous RNA (ceRNA) by sponging miR-3646, which leads to the derepression of Frizzled-7 (FZD7) and subsequent activation of the Wnt/β-catenin signaling pathway. These findings identify USP30-AS1 as a critical promoter of stemness, chemoresistance, and metastasis in BCSCs via the miR-3646/FZD7/Wnt axis, suggesting it is a potential therapeutic target for breast cancer intervention.
23 days ago
Journal
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CTNNB1 (Catenin (cadherin-associated protein), beta 1) • CD44 (CD44 Molecule) • POU5F1 (POU Class 5 Homeobox 1) • ALDH1A1 (Aldehyde Dehydrogenase 1 Family Member A1) • FZD7 (Frizzled Class Receptor 7) • USP30-AS1 (USP30 Antisense RNA 1)
RRSM is a potential prognostic predictor for STS and lays a foundation for early intervention of high-risk STS patients. The expression of genes FZD7, ITPKA, and PRKAG1 may guide STS treatment decisions.
1 month ago
Journal
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COL6A3 (Collagen Type VI Alpha 3 Chain) • PRKAG1 (Protein Kinase AMP-Activated Non-Catalytic Subunit Gamma 1) • FZD7 (Frizzled Class Receptor 7) • ITPKA (Inositol-Trisphosphate 3-Kinase A)
In summary, we provide here the proof-of-principle that targeting FZDs with small molecule compounds is possible and effective. Future hit optimization and functional validation in disease-relevant in vitro and in vivo models will pave the way towards clinical exploration.
To model acquired resistance, PC-9 cells were exposed to vinorelbine or paclitaxel for 18 weeks-approximating the clinical duration of four adjuvant chemotherapy cycles-and subsequent drug sensitivity and signaling pathway alterations were assessed using cell viability assays, RNA sequencing, and immunoblotting. These findings suggest that CaMKII plays a critical role in EGFR-TKI resistance. This study underscores the importance of optimizing the timing of EGFR-TKI administration in the therapeutic sequence for EGFR-mutated NSCLC.
Despite the cellular heterogeneity of MMTV-Wnt1 tumors, treatment with a Fzd7-specific antibody-drug conjugate significantly suppresses tumor growth, suggesting that Fzd7-expressing cells are critical drivers of tumor progression. These findings show that Fzd7 marks a population of putative tumor-initiating cells and that targeting Fzd7 offers a promising therapeutic strategy for breast cancer.
In vivo, treatment with anti-FZD7-288.1 significantly inhibited WT xenograft growth, resulting in reduced tumor volume. These findings demonstrate that FZD7 is a critical driver of Wilms tumor progression and support antibody-mediated FZD7 blockade as a promising therapeutic strategy.
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.
5 months ago
Journal
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TGFB1 (Transforming Growth Factor Beta 1) • THY1 (Thy-1 membrane glycoprotein) • NANOG (Nanog Homeobox) • FZD7 (Frizzled Class Receptor 7) • WNT3 (Wnt Family Member 3)
Extracellular vesicles (EVs), secreted under hypoxia, can deliver modified bioactive cargo that reprograms recipient cells...These findings show that hypoxia-driven EVs can propagate pro-metastatic signalling in less aggressive and normal prostate cells. The findings highlight EVs as a potential therapeutic target in PCa progression.
Mechanistically, FPR3 upregulates FZD7 and CCDC88C, leading to activation of the intracellular Wnt/PCP pathway and downstream JNK signaling, thereby promoting TAM development. Collectively, our study identifies FPR3 as a novel marker of immunosuppressive TAMs, elucidates its mechanistic role in macrophage plasticity, and offers new insights into potential therapeutic strategies for targeting the tumor microenvironment in GA.