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Bone Regeneration Effect of Cassia occidentalis Linn. Extract and Its Isolated Compounds
Published in Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay, Phytochemistry of Plants of Genus Cassia, 2021
Brijesh Kumar, Vikas Bajpai, Vikaskumar Gond, Subhashis Pal, Naibedya Chattopadhyay
In cultures of rat chondrocytes, emodin suppressed the cytotoxic impact of IL-1β, downregulated the expressions of MMP-1 and MMP-13 and inhibited the ERK and Wnt/β-catenin signaling (Liu et al., 2018). In murine chondrogenic cell line, ATDC5, emodin treatment caused the loss of cell viability at 15- and 20 μM. However, at 10 μM, emodin blocked the LPS-induced apoptosis of and production of proinflammatory cytokines (TNFα, IL-6 and MCP1) from ATDC5 cells. The pro-survival, anti-apoptotic and anti-inflammatory roles of emodin in ATDC5 were likely regulated by the long noncoding RNA, taurine upregulated gene 1-mediated notch and NFκB pathways (Liang and Ren, 2018). Given this action mechanism of emodin chondrocytes, a salutary role of this compound in OA is surmised.
Targeting Subgroup-specific Cancer Epitopes for Effective Treatment of Pediatric Medulloblastoma
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Sidharth Mahapatra, Naveenkumar Perumall
Thus, drugs that specifically target WNT/β-catenin signaling may provide a preferred alternative approach to the current conventional cytotoxic therapies. However, WNT subgroup MB possesses the best prognostic profile amongst medulloblastomas with an approximate 90% five-year event-free survival [2, 34]. As a result, efforts are now underway to study the effects of potentially limiting cytotoxic therapies (NCT02066220, NCT01878617, and NCT02724579) [8, 35]. Hence, these targeted therapeutics have yet to find their way to clinical trials. That said, this subset of patients may benefit from further restrictions in cytotoxic therapies with the addition of these promising therapeutic options.
Colon cancer: pathology and natural history
Published in A. R. Genazzani, Hormone Replacement Therapy and Cancer, 2020
The region of the APC protein between residues 1014 and 1210 has the property of associating with α- and ß-catenins15 (Figure 4). Catenins are a group of cytoplasmic proteins that were identified primarily because of their association with the cell adhesion molecule E-cadherin15. ß-Catenin shares substantial homology with armadillo, a Drosophila segment polarity gene product involved in signal transduction15. α-Catenin, which also binds actin, is thus thought to link the adherens junction and the APC protein to the actin cytoskeleton.
Suspended cell lines for inactivated virus vaccine production
Published in Expert Review of Vaccines, 2023
Jiayou Zhang, Zhenyu Qiu, Siya Wang, Zhenbin Liu, Ziling Qiao, Jiamin Wang, Kai Duan, Xuanxuan Nian, Zhongren Ma, Xiaoming Yang
The calcium dependent cell adhesins (cadherin) family is one of the earliest adhesion molecules that Takeichi discovered to mediate cell aggregation. In the presence of Ca2+, it can resist protease hydrolysis. The connection between the cytoskeleton transmembrane protein E-cadherin (also known as uvomorulin, L-CAM, cell CAM 120/80, or ARC-1) and actin filament is the key to cell-cell adhesion. Cells lacking E-cadherin expression do not aggregate or adhere to each other because the production of cadherin-catenin adhesion complexes is affected [106]. α-Catenin is a key subunit of the cadherin catenin adhesion complex, which affects cell-cell adhesion. In the absence of stable α-Catenin expression in poorly differentiated cell lines, the addition of α- Catenin cDNA will increase Ca2+-dependent cell-cell aggregation, indicating that α-Catenin directly leads to the loss of cell-cell adhesion in some cell lines [109]. In α-Catenin-ablated keratinocytes, cell-cell connection defects could be observed using immunofluorescence microscopy along with excessive cell proliferation [110].
Synthesis and biological evaluation of thieno[3,2-c]pyrazol-3-amine derivatives as potent glycogen synthase kinase 3β inhibitors for Alzheimer’s disease
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Ning Yan, Xiao-Long Shi, Long-Qian Tang, De-Feng Wang, Xun Li, Chao Liu, Zhao-Peng Liu
GSK-3β is implicated in the Wnt/β-catenin signalling pathway, which plays an important role in neuronal development29. GSK-3β, together with adenomatous polyposis coli (APC), Axin, and casein kinase 1 (CK1), form a ploy-protein complex that regulates the hyperphosphorylation of β-catenin. Phospho-β-catenin is recognised by ubiquitin and degraded by proteasomes52–54. Pharmacological inhibition of GSK-3β leads to the activation and stabilisation of β-catenin, subsequently resulting in the accumulation of β-catenin in cytoplasm55–57. The activation of Wnt/β-catenin signalling pathway can promote synaptic growth, alleviate spatial memory impairment and neurodegeneration in Alzheimer’s models 58–60. Moreover, β-catenin also plays a pivotal role in cell adhesion complexes. The combination of β-catenin and N-cadherin elevates cell-to-cell interactions which is prerequisite for neuronal differentiation61,62. Therefore, we further evaluated the effect of 16b on β-catenin. In agreement with its GSK-3β inhibitory activity on SH-SY5Y cells, 16b increased β-catenin abundance in a dose-dependent manner. As shown in Figure 6(B), after treatment with 16b at the concentration of 5 μM, 10 μM and 20 μM, the β-catenin/GADPH ratio increased from 0.41 of the control to 0.54, 0.64, 0.76, respectively.
Mechanism of the Fibroblast Growth Factor 23/α-Klotho Axis in Peripheral Blood Mononuclear Cell Inflammation in Alzheimer’s Disease
Published in Immunological Investigations, 2022
Baoshan Li, Min Zhou, Jing Peng, Qiao Yang, Jingxin Chu, Ruoqing Li, Yi Jiang
A previous study has shown that the Wnt signaling has a regulatory effect on microglial inflammation in AD (Yang and Zhang 2020). Therefore, we investigated the Wnt/β-catenin pathway impact on cell inflammation in AD using DKK1. Our findings showed that DKK1 treatment increased inflammatory cytokine levels. These findings are consistent with our previous observation that the inhibition of the Wnt/β-catenin pathway contributes highly to the enhanced neuroinflammation in some neurodegenerative diseases, such as AD (Jiang et al. 2016). In addition, we observed that inhibition of the Wnt/β-catenin pathway reversed the effects of FGF23 knockdown and α-Klotho overexpression on reducing AD-induced cell inflammation. Similarly, the Wnt/β-catenin pathway activation is intrinsically related to the reduced FGF23 level and elevated Klotho value, accompanied by the suppressed inflammation in a high phosphorus and LPS-induced in vitro experiment (Rodriguez-Ortiz et al. 2020). From the above studies, it can be concluded that FGF23 knockdown and α-Klotho overexpression reduce AD-induced inflammation by activating the Wnt/β-catenin pathway in PBMCs.