Mar 28, 2016
Targeting Cancer Stem Cells with NonToxic Therapies
This article is copyrighted by Jeffrey Dach MD, 2013 Republished with permission from JeffreyDachMD.com
drdach
90 minSearch Research
Search across 105,000+ research abstracts, articles, substances, health topics, keywords, and actions.
Found 76 results for "wnt catenin signaling pathway modulation"
Articles (4)
Apr 09, 2021
Pomegranate: Evidence-Based Benefits of This Antioxidant Superstar
Pomegranate, with its characteristic red arils, is small but mighty when it comes to substantial
DianeFulton
14 min
Sep 03, 2024
Grape Exosomes: Nature's Nanoparticles for Cellular Communication and Regenerative Healing
Tiny particles from grapes may hold the key to unlocking profound healing effects throughout the
GMI Research Group
7 min
Aug 12, 2019
Plant-Derived Exosomes as Cross-Species Messengers and Beacons of Epigenetics
Cross-talk between plant and animal cells may be accomplished via microRNA-carrying exosomes, gene
AliLeVere
14 minAbstracts (72)
View allChlorogenic acids inhibit adipogenesis: implications of Wnt/ β-catenin signaling pathway.
In our previous in vitro study, we found that chlorogenic acid (CGA) inhibited adipocyte differentiation and triglyceride (TG) accumulation, but the underlying mechanism is still unclear. Accumulative genetic evidence supports that canonical Wnt signaling is a key modulator on adipogenesis.. In this study, 3T3-L1 cells were induced adipogenic differentiation and then treated with CGA. We investigate the effect of CGA in inhibiting adipogenesis and evaluate its role in modulating Wnt10b (wingless integration1 10b),-catenin, glycogen synthase kinase-3(GSK-3), and peroxisome proliferator-activated receptor(PPAR-) involved in the Wnt (wingless integration1)/-catenin signaling pathway.. The result showed that after CGA treatment, lipid accumulation and TG level decreased significantly in 3T3-L1 cells, indicating that CGA could inhibit adipogenesis. In addition, CGA repressed the induction of adipocyte differentiation biomarkers as PPAR-, adipocyte protein 2 (aP2), fatty acid synthase (FAS), and lipoprotein lipase (LPL), and the secretion of GSK-3in a dose-dependent manner upregulated the expression of-catenin and Wnt10b both in gene and protein levels. Moreover, CGA induced phosphorylation of GSK-3and promoted the accumulation of free cytosolic-catenin in 3T3-L1 adipocytes.. Overall, these findings gave us the implications that CGA inhibits adipogenesis via the canonical Wnt signaling pathway.
Mengting Liu, Jian Qin, Jing Cong, Yubin Yang, Int J Endocrinol
In Vitro Study
Nature-derived compounds modulating Wnt/ β -catenin pathway.
The Wnt/-catenin signaling is a conserved pathway that has a crucial role in embryonic and adult life. Dysregulation of the Wnt/-catenin pathway has been associated with diseases including cancer, and components of the signaling have been proposed as innovative therapeutic targets, mainly for cancer therapy. The attention of the worldwide researchers paid to this issue is increasing, also in view of the therapeutic potential of these agents in diseases, such as Parkinson's disease (PD), for which no cure is existing today. Much evidence indicates that abnormal Wnt/-catenin signaling is involved in tumor immunology and the targeting of Wnt/-catenin pathway has been also proposed as an attractive strategy to potentiate cancer immunotherapy. During the last decade, several products, including naturally occurring dietary agents as well as a wide variety of products from plant sources, including curcumin, quercetin, berberin, and ginsenosides, have been identified as potent modulators of the Wnt/-catenin signaling and have gained interest as promising candidates for the development of chemopreventive or therapeutic drugs for cancer. In this review we make an overview of the nature-derived compounds reported to have antitumor activity by modulating the Wnt/-catenin signaling, also focusing on extraction methods, chemical features, and bio-activity assays used for the screening of these compounds.
Gianluca Sferrazza, Marco Corti, Gloria Brusotti, Pasquale Pierimarchi, Caterina Temporini, Annalucia Serafino, Enrica Calleri, Acta Pharm Sin B
Review
Gastrodin attenuates proliferation and inflammatory responses in activated microglia through Wnt/β-catenin signaling pathway.
Microglia contribute to the regulation of neuroinflammation and play an important role in the pathogenesis of brain disorders. Thus, regulation of neuroinflammation triggered by activation of microglia has become a promising therapeutic strategy. Here, we investigated the beneficial effects of Gastrodin in activated microglia and analyzed the underlying molecular mechanisms. Microglia activation was regulated by Gastrodin not only in terms of microglia population size but also production of inflammatory mediators. Gastrodin inhibited the expression of inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), cyclin-D1 and Ki67 in lipopolysaccharide (LPS)-stimulated BV-2 or primary microglia. Gastrodin also suppressed the expression of iNOS and Ki67 in activated microglia in three-day-old LPS-injected postnatal rats. In addition, the present results have shown that Gastrodin inhibited LPS-induced phosphorylation of glycogen synthase kinase-3β (GSK-3β) at Ser 9 and β-catenin activity. We further extended our investigation to determine whether Wnt/β-catenin signaling pathway was involved in the anti-inflammatory and anti-proliferation function of Gastrodin. β-Catenin antagonist (XAV939) was used to block LPS-mediated upregulation of iNOS, TNF-α, cyclin-D1, nitric oxide (NO) and the number of cells in the G2/M+S phase of cell cycle. Moreover, treatment with LiCl, a special Wnt/β-catenin pathway agonist significantly blocked Gastrodin-mediated down-regulation of iNOS, TNF-α,cyclin-D1, NO and the number of cells in the G2/M+S phase of cell cycle in LPS-stimulated BV-2 microglia. Taken together, the present results suggested that Gastrodin mediated anti-inflammatory and anti-proliferation effects in activated microglia by modulating the Wnt/β-catenin signaling pathway.
Yue-Yi Yao, Li-Gong Bian, Ping Yang, Yue Sui, Run Li, Yuan-Li Chen, Lin Sun, Qing-Long Ai, Lian-Mei Zhong, Di Lu, Brain Res
In Vitro Study
Astaxanthin inhibits NF-κB and Wnt/β-catenin signaling pathways via inactivation of Erk/MAPK and PI3K/Akt to induce intrinsic apoptosis in a hamster model of oral cancer.
BACKGROUND: The oncogenic transcription factors NF-κB and β-catenin, constitutively activated by upstream serine/threonine kinases control several cellular processes implicated in malignant transformation including apoptosis evasion. The aim of this study was to investigate the chemopreventive effects of astaxanthin, an antioxidant carotenoid, inthe hamster buccal pouch (HBP) carcinogenesis model based on its ability to modulate NF-κB and Wnt signaling pathways and induce apoptosis. METHODS: We determined the effect of dietary supplementation of astaxanthin on the oncogenic signaling pathways - NF-κB and Wnt/β-catenin, their upstream activator kinases - Erk/MAPK and PI-3K/Akt, and the downstream event - apoptosis evasion by real-time quantitative RT-PCR, western blot, and immunohistochemical analyses. RESULTS: We found that astaxanthin inhibits NF-κB and Wnt signaling by downregulating the key regulatory enzymes IKKβ and GSK-3β.Analysis of gene expression and docking interactions revealed that inhibition of these pathways may be mediated via inactivation of the upstream signaling kinases Erk/Akt by astaxanthin. Astaxanthin also induced caspase-mediated mitochondrial apoptosis by downregulating the expression of antiapoptotic Bcl-2, p-Bad, and survivin and upregulating proapoptotic Bax and Bad, accompanied by efflux of Smac/Diablo and cytochrome-c into the cytosol, and induced cleavage of poly (ADP-ribose) polymerase (PARP). CONCLUSIONS: The results provide compelling evidence that astaxanthin exerts chemopreventiveeffects by concurrently inhibiting phosphorylation of transcription factors and signaling kinases and inducing intrinsic apoptosis. GENERAL SIGNIFICANCE: Astaxanthin targets key molecules in oncogenic signaling pathways and induces apoptosis and is a promising candidate agent for cancer prevention and therapy.
K Kavitha, J Kowshik, T Kranthi Kiran Kishore, Abdul Basit Baba, S Nagini, Biochim Biophys Acta
In Vitro Study
Hydrolyzed egg yolk peptide prevented osteoporosis by regulating Wnt/β-catenin signaling pathway.
Hydrolyzed egg yolk peptide (YPEP) was shown to increase bone mineral density in ovariectomized rats. However, the underlying mechanism of YPEP on osteoporosis has not been explored. Recent studies have shown that Wnt/β-catenin signaling pathway and gut microbiota may be involved in the regulation of bone metabolism and the progression of osteoporosis. The present study aimed to explore the preventive effect of the YPEP supplementation on osteoporosis in ovariectomized (OVX) rats and to verify whether YPEP can improve osteoporosis by regulating Wnt/β-catenin signaling pathway and gut microbiota. The experiment included five groups: sham surgery group (SHAM), ovariectomy group (OVX), 17-βestradiol group (E2: 25µg /kg/d 17β-estradiol), OVX with low-dose YPEP group (LYPEP: 10 mg /kg/d YPEP) and OVX with high-dose YPEP group (HYPEP: 40 mg /kg/d YPEP). In this study, all the bone samples used were femurs. Micro-CT analysis revealed improvements in both bone mineral density (BMD) and microstructure by YPEP treatment. The three-point mechanical bending test indicated an enhancement in the biomechanical properties of the YPEP groups. The serum levels of bone alkaline phosphatase (BALP), bone gla protein (BGP), calcium (Ca), and phosphorus (P) were markedly higher in the YPEP groups than in the OVX group. The LYPEP group had markedly lower levels of alkaline phosphatase (ALP), tartrate-resistant acid phosphatase (TRAP) and C-terminal telopeptide of type I collagen (CTX-I) than the OVX group. The YPEP groups had significantly higher protein levels of the Wnt3a,β-catenin, LRP5, RUNX2 and OPG of the Wnt/β-catenin signaling pathway compared with the OVX group. Compared to the OVX group, the ratio of OPG/RANKL was markedly higher in the LYPEP group. At the genus level, there was a significantly increase in relative abundance of Lachnospiraceae_NK4A136_group and a decrease in Escherichia_Shigella in YPEP groups, compared with the OVX group. However, in the correlation analysis, there was no correlation between these two bacteria and bone metabolism and microstructure indexes. These findings demonstrate that YPEP has the potential to improve osteoporosis, and the mechanism may be associated with its modulating effect on Wnt/β-catenin signaling pathway.
Chuanjing Chen, Ludi Huang, Yuanyuan Chen, Jin Jin, Ze Xu, Fei Liu, Kelei Li, Yongye Sun, Sci Rep
Animal Study
