Gentaur Pub

#39373865   2024/10/07 To Up

Long noncoding RNA MEG3: an active player in fibrosis.

Fibrosis, characterized by excess accumulation of extracellular matrix components, disrupts normal tissue structure and causes organ dysfunction. Long noncoding RNAs (lncRNAs) are a subset of RNAs longer than 200 nucleotides that are not converted into proteins. The increasing research indicated that lncRNA maternally expressed gene 3 (MEG3) was dysregulated in the pathologic process of fibrosis in several tissues. LncRNA MEG3 was revealed to regulate the expression of target proteins or serve as a miRNAs sponge to control the development of fibrosis, which was involved in NF-ҡB, PI3K/AKT, JAK2/STAT3, Wnt/β-catenin, ERK/p38, and Hh pathway. Importantly, the interference of MEG3 level ameliorated fibrosis. The present review summarized available studies of lncRNA MEG3 in fibrosis, which is helpful for a deeper understanding of the roles of MEG3 in fibrosis.
Xiaoying Jiang

2656 related Products with: Long noncoding RNA MEG3: an active player in fibrosis.

200ul100 μg100 μg0.1ml100 μg100ug100 μg1 Set1 Set4 Membranes/Box1 Set100 μg

Related Pathways

#39372730   2024/08/23 To Up

Restoring mechanophenotype reverts malignant properties of ECM-enriched vocal fold cancer.

Increased extracellular matrix (ECM) and matrix stiffness promote solid tumor progression. However, mechanotransduction in cancers arising in mechanically active tissues remains underexplored. Here, we report upregulation of multiple ECM components accompanied by tissue stiffening in vocal fold cancer (VFC). We compare non-cancerous (NC) and patient- derived VFC cells - from early (mobile, T1) to advanced-stage (immobile, T3) cancers - revealing an association between VFC progression and cell-surface receptor heterogeneity, reduced laminin-binding integrin cell-cell junction localization and a flocking mode of collective cell motility. Mimicking physiological movement of healthy vocal fold tissue (stretching/vibration), decreases oncogenic nuclear β-catenin and YAP levels in VFC. Multiplex immunohistochemistry of VFC tumors uncovered a correlation between ECM content, nuclear YAP and patient survival, concordant with VFC sensitivity to YAP-TEAD inhibitors in vitro. Our findings present evidence that VFC is a mechanically sensitive malignancy and restoration of tumor mechanophenotype or YAP/TAZ targeting, represents a tractable anti-oncogenic therapeutic avenue for VFC.
Jasmin Kaivola, Karolina Punovuori, Megan R Chastney, Yekaterina A Miroshnikova, Hind Abdo, Fabien Bertillot, Fabian Krautgasser, Jasmin Di Franco, James R W Conway, Gautier Follain, Jaana Hagström, Antti Mäkitie, Heikki Irjala, Sami Ventelä, Hellyeh Hamidi, Giorgio Scita, Roberto Cerbino, Sara A Wickström, Johanna Ivaska

1424 related Products with: Restoring mechanophenotype reverts malignant properties of ECM-enriched vocal fold cancer.

Related Pathways

#39371752   2024/09/04 To Up

Graph Neural Network-Based Drug Gene Interactions of Wnt/β-Catenin Pathway in Bone Formation.

Introduction The Wnt/β-catenin pathway is crucial for bone formation and remodeling, regulating osteoblast differentiation, bone remodeling, and skeletal homeostasis. Dysregulation of the Wnt/β-catenin pathway is linked to bone-related diseases like osteoporosis, osteoarthritis, and osteosarcoma. The strategies to modulate this pathway include Wnt agonists, inhibitors, and small molecules. Graph neural networks (GNNs) have shown potential in understanding drug-gene interactions, providing accurate predictions, identifying novel drug-target pairs, and enabling personalized drug therapy. So we aim to predict GNN-based drug-gene interactions of Wnt/β-catenin pathway in bone formation. Methodology The drug-gene interactions of Wnt signaling were annotated and preprocessed using Cytoscape, a powerful tool for building drug-gene interactions. Data was imported, nodes representing drugs and genes were created, and edges represented their interactions. GNNs were used to prepare data for nodes, genes, and drugs. GNNs are designed to operate on graph-structured data, capable of learning complex relationships between the nodes. The architecture consists of several steps: graph representation, message passing, node representation update, graph-level readout, and prediction or output. A data representation system is a GNN with an Adam optimizer, 100 epochs, a learning rate of 0.001, and entropy loss. Results The network has 108 nodes, 134 edges, and 2.444 neighbors, with a diameter of 4, radius of 2, and characteristic path length of 2.635. It lacks clustering, sparse connectivity, wide connection variation, and moderate centralization. The GNN model's drug-gene interactions demonstrate high precision, recall, F1 score, and accuracy, with a high sensitivity to true-positives and low false-negatives. Conclusion The study employs a GNN model to predict drug-gene interactions in the Wnt/β-catenin pathway, demonstrating high precision and accuracy, but further research is needed.
Pradeep Kumar Yadalam, R Ramya, Raghavendra Vamsi Anegundi, Shubhangini Chatterjee

2585 related Products with: Graph Neural Network-Based Drug Gene Interactions of Wnt/β-Catenin Pathway in Bone Formation.

2 Pieces/Box100 assays2 Pieces/Box5ug2 Pieces/Box100 assays2 Pieces/Box2 Pieces/Box100 assays2 Pieces/Box100 assays

Related Pathways

#39371729   2024/09/06 To Up

Epithelial-Mesenchymal Transition Indexes in Triple-Negative Breast Cancer Progression and Metastases.

Background Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer characterized by the lack of expression of estrogen and progesterone receptors and the absence of HER2 protein overexpression or gene amplification. How TNBC becomes so aggressive at the molecular level is not yet fully understood. The epithelial-mesenchymal transition (EMT) has been increasingly recognized as playing a pivotal role in cancer progression and metastasis. This study aimed to elucidate the connection between TNBC progression with EMT-related markers, including vimentin, beta-catenin, and E-cadherin. Methodology Rigorous immunohistochemical analysis was employed to assess the expression of vimentin, beta-catenin, and E-cadherin in primary tumors, tumor buds, and lymph node metastases (LNMs) from 137 cases with an invasive ductal carcinoma triple-negative phenotype diagnosed between 2018 and 2024. The EMT index, which was especially important in our work, is the sum of vimentin and beta-catenin expression divided by that of E-cadherin. Estimated Pearson correlation, multiple linear regression, and Kruskal-Wallis tests were used to determine the relationships of the EMT index with tumor buds and tumor-infiltrating lymphocytes (TILs). Results Vimentin highly correlated within separate regions of interest with Pearson correlation ranging from 0.90 to 0.92 (p < 0.001). Strong negative correlations between E-cadherin and vimentin (r = -0.81 to - 0.89, p < 0.001) showed its role in preserving the epithelial phenotype. The presence of tumor buds, aggregates, or clusters of cancer cells shed from the primary tumor mass invading the connective tissue showed very strong associations with the EMT index (r = 0.91, p < 0.001). Its presence is suggestive of aggressive disease and may identify a high-risk subpopulation that may benefit from more active surveillance or adjuvant treatment. Similarly, TILs correlated inversely with the EMT index (r = -0.90, p < 0.001). The most significant predictor of the EMT index, i.e., vimentin, had a model R-squared value of 1.000 in the regression analysis. Conclusions This study brings to light the importance of EMT-related markers in TNBC progression, with special emphasis on tumor buds as possible prognostic indicators for aggressive disease. The negative correlation of TILs with the EMT index indicates that an effective immune response could antagonize EMT-mediated tumor progression. These results suggest that EMT-based treatments in TNBC should be designed from a multimarker perspective by including interactions among several markers to optimize predictions and therapeutics. The results hold the potential to set future research directions and actionable outcomes that could influence clinical utility in the battle against TNBC.
Shota Kepuladze, George Burkadze, Irakli Kokhreidze

1701 related Products with: Epithelial-Mesenchymal Transition Indexes in Triple-Negative Breast Cancer Progression and Metastases.

Related Pathways

#39370687   2024/10/06 To Up

Ethionine-induced S-adenosylmethionine deficiency suppressed H3K27me3 and cell differentiation during neural tube development in mice.

S-adenosylmethionine (SAM) as a major methyl donor plays a key role in methylation modification in vivo, and its disorder was closely related to neural tube defects (NTDs). However, the exact mechanism between SAM deficiency and NTDs remained unclearly. Hence, we investigated the association between histone methylation modification and cell differentiation in NTDs mice induced by SAM deficiency. The levels of SAM and SAH (S-adenosylhomocysteine) were determined by enzyme linked immunosorbent assay (ELISA). The level of histone methylation, β-catenin were analyzed by Western blot, reversing transcription and quantitative PCR (RT-qPCR) and immunofluorescence. The results showed that the incidence rate of NTDs induced by ethionine were 46.2%. Post treatment of ethionine combined with SAM, the incidence rate of NTDs was reduced to 26.2%. The level of SAM was significantly decreased (p < 0.05) and a reduction in the SAM/SAH ratio was observed after entionine treatment. The SAM deficiency caused the reduction of H3K27me3 modifications and the elevated UTX activity (p < 0.05), and inhibited the expressions of β-catenin. The differentiations of NSCs into neurons and oligodendrocytes were inhibited under SAM deficiency (p < 0.05). These results indicated that the SAM deficiency led to reduce H3K27me3 modifications, prevented the β-catenin signaling pathway and NSCs differentiation, which provided an understanding of the novel function of epigenetic regulation in NTDs.
Li Zhang, Xiaona Zhang, Yurong Liu, Kaixin Wei, Huijing Ma, Li Xia, Rui Cao, Yuqing Sun, Ronghua Zheng, Xiuwei Wang, Bingmei Chang

1513 related Products with: Ethionine-induced S-adenosylmethionine deficiency suppressed H3K27me3 and cell differentiation during neural tube development in mice.

96 assays1 mg1 mg100 μg400 ug400 ug1.00 flask1mg100ug Lyophilizedcase

Related Pathways

#39370517   2024/10/06 To Up

Interferon regulatory factor 7 alleviates the experimental colitis through enhancing IL-28A-mediated intestinal epithelial integrity.

The incidence of inflammatory bowel disease (IBD) is on the rise in developing countries, and investigating the underlying mechanisms of IBD is essential for the development of targeted therapeutic interventions. Interferon regulatory factor 7 (IRF7) is known to exert pro-inflammatory effects in various autoimmune diseases, yet its precise role in the development of colitis remains unclear.
Furong Qing, Hongbo Tian, Biyao Wang, Bingyu Xie, Lina Sui, Xiaoyan Xie, Wenji He, Tiansheng He, Yumei Li, Liangmei He, Qin Guo, Zhiping Liu

2984 related Products with: Interferon regulatory factor 7 alleviates the experimental colitis through enhancing IL-28A-mediated intestinal epithelial integrity.

100 0.1 mg0.1 mg 1 G200ug250ul 100ul100 μg 10 MG25 g5mg

Related Pathways

#39370268   // To Up

Asperuloside Suppresses the Development of Depression through Wnt3α/GSK-3β Signal Pathway in Rats.

Depressive disorder is the most common mental disorder with significant economic burden and limited treatments. Traditional Chinese medicine monomer has emerged as a promising non-pharmacological treatment for reducing depressive symptoms. The aim of this study was to investigate the antidepressant-like effects of asperuloside (ASP) and its mechanism. The depression-like behaviors of chronic unpredictable mild stress (CUMS)-exposed rats were evaluated by behavioral tests. At the same time, the behaviors of rats treated with different concentrations of ASP (10, 20, 40 mg/kg) were also evaluated. RNA sequencing was performed to screen for dysregulated genes following ASP treatment. The Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis was performed to state the enriched pathways. Protein expression was detected by Western blotting. With the increase of ASP concentration (over 20 mg/kg), the depression-like behaviors of the rats were alleviated, which was manifested as the increase of the number of entries in the central zone, decrease of immobility time, and the increase of swimming time, sucrose preference, and body weight. ASP activated the Wnt3α/glycogen synthase kinase 3β (GSK-3β)/β-catenin signaling pathway in vivo. Knockdown of β-catenin reversed the effects of ASP on regulating depression-like behaviors. ASP alleviates depression-like behaviors by activating the Wnt3α/GSK-3β/β-catenin signaling pathway, indicating that ASP may be a potential therapeutic drug for treatment of depression.
Li Yin, Chengshu Lu, Shiyuan Zeng, Deqi Jiang, Guofang Zeng, Huakun Wang

2726 related Products with: Asperuloside Suppresses the Development of Depression through Wnt3α/GSK-3β Signal Pathway in Rats.

14 inhibitors2 Pieces/Box2 Pieces/Box7 inhibitors2 Pieces/Box2 Pieces/Box2 Pieces/Box11 inhibitors2 Pieces/BoxInhibitors2 Pieces/Box2 Pieces/Box

Related Pathways

#39369835   2024/10/04 To Up

Runx2 silencing sensitized human renal cell carcinoma cells to ABT-737 apoptosis.

The prognostic value of Runt-related transcription factor 2 (Runx2) and its involvement in cell growth and motility have been reported in patients diagnosed with renal cell carcinoma (RCC). Since Runx2 may have the potential to be a target for the purpose of antitumor intervention, there is an urgent need to gain insight into its oncogenic properties. Using human 786-O, Caki-1 and ACHN RCC cells as models, the silencing of cellular Runx2 expression brought about a reduction in cyclin D1 and β-catenin expression, cell growth and migration without any significant cell death. Runx2-silenced cells turned into apoptosis vulnerable in the presence of ABT-737, a BH3 mimetic Bcl-2 inhibitor. Data from biochemical and molecular studies have revealed a positive correlation between Runx2 expression and Akt phosphorylation, Mcl-1 expression, and fibronectin expression. Results of genetic silencing studies have indicated the potential involvement of Mcl-1 and fibronectin in the decision of RCC cell ABT-737 resistance and sensitivity. The regulatory roles of the PI3K/Akt axis in the expression of Mcl-1 and fibronectin were suggested by means of the results taken from experiments involving pharmacological study of the PI3K/Akt. Since overexpression and prognostic roles of Runx2, activated Akt, Mcl-1, fibronectin, cyclin D1, and β-catenin have been revealed in RCC, it is important to explore the precise mechanisms underlying Runx2 oncogenic effects. Although the linking details between Runx2 and PI3K/Akt have yet to be identified, our findings suggest that Mcl-1 and fibronectin are downstream effectors of Runx2 via a regulatory axis of the PI3K/Akt and their promotion of cell growth, migration, and ABT-737 resistance in RCC cells.
Yen-Chuan Ou, Tung-Min Yu, Jian-Ri Li, Chih-Cheng Wu, Jiaan-Der Wang, Su-Lan Liao, Wen-Ying Chen, Yu-Hsiang Kuan, Chun-Jung Chen

1582 related Products with: Runx2 silencing sensitized human renal cell carcinoma cells to ABT-737 apoptosis.

1.00 flask1.00 flask1.00 flask0.1 mg5 x 50 ug1.00 flask1.00 flask100 ug/vial21.00 flask0.1ml (1mg/ml)1mg

Related Pathways

#39368400   2024/10/04 To Up

IMP3, CDK4, MDM2 and β-catenin expression in Enchondroma and Central Chondrosarcoma: Diagnostic and prognostic utility.

The role of IMP3, CDK4, MDM2 and β-catenin proteins in Enchondroma and Central Chondrosarcoma is not totally understood. The aim of this study is to evaluate the immunoexpression of these proteins, associating histological grade, clinical data and prognosis to these tumors.
Daniele Moraes Losada, Maurício Etchebehere, Francisco Fontes Cintra, Eliane Maria Ingrid Amstalden

2973 related Products with: IMP3, CDK4, MDM2 and β-catenin expression in Enchondroma and Central Chondrosarcoma: Diagnostic and prognostic utility.

1,000 tests100ul1 mg1000 tests100ug50 ug 100ug100 mg10 mg100ul5mg

Related Pathways

#39368268   2024/09/30 To Up

Cephalomannine reduces radiotherapy resistance in non-small cell lung cancer cells by blocking the β-catenin-BMP2 signaling pathway.

The management of non-small cell lung cancer (NSCLC) often includes the use of radiotherapy, with individual outcomes being impacted by the tumor's response to this treatment modality. Cephalomannine (CPM), a taxane diterpenoid found in Taxus spp, has been found to have anti-tumor activity. This study was aim to the explore the role and mechanism by which CPM affects radiotherapy resistance in NSCLC.
Suhong An, Xiaoping Xu, Yanhong Bao, Fang Su, Yiqian Jiang

1017 related Products with: Cephalomannine reduces radiotherapy resistance in non-small cell lung cancer cells by blocking the β-catenin-BMP2 signaling pathway.

1.5 x 10^6 cells2 Pieces/Box1.5x10(6) cells

Related Pathways