Combinatorial chemistry & high throughput screening最新文献

Objective: Colorectal Cancer (CRC) has attracted much attention due to its high mortality and morbidity. Cordycepin, also known as 3'-deoxyadenosine (3'-dA), exhibits many biological functions, including antibacterial, anti-inflammatory, antiviral, anti-tumor, and immunomodulatory effects. It has been proven to show anticancer activity in both laboratory research studies and living organisms. However, the molecular mechanism of the effect of cordycepin on CRC remains unclear.

Methods: The genes associated with cordycepin and colorectal cancer have been identified by comparing the toxicogenomics database (CTD) and GeneCards database. The common genes between cordycepin and CRC have been identified using the Venny tool. The Protein-protein Interaction (PPI) network has been drawn using the STRING database. GO and KEGG enrichment analyses of the intersecting genes have been followed by experimental validation, both in vitro and in vivo.

Results: 24 drug targets have been screened using the CTD database and 1490 disease targets have been obtained from the GeneCards database and GO and KEGG analyses. The effect of cordycepin on the proliferation of SW480 cells has been assessed using CCK-8. The related results have indicated cordycepin to inhibit the proliferation of SW480 cells, promote apoptosis, and activate the p53 signal pathway. The findings obtained from in vivo experiments have been found to be consistent with those obtained from in vitro studies.

Conclusion: Our findings have elucidated an effective way to search for cordycepin's potential mechanism of effect on CRC therapy by employing the network pharmacology and experiment. We have predicted that cordycepin can inhibit tumor growth by regulating the apoptosis pathway. This study has offered valuable insights into the potential mechanism of the effect of cordycepin on CRC and provided a theoretical basis for further validation of its clinical application.

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Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article has been withdrawn.

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The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php

Bentham science disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article has been withdrawn.

Bentham Science apologizes to the readers of the journal for any inconvenience this may have caused.

The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php

Bentham science disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

Background: Shengyang Yiwei Decoction showed efficacy in idiopathic membranous nephropathy treatment, and this study aimed to assess the underlying molecular mechanisms.

Methods: Rats with passive Heymann nephritis were divided into the model group, the Shengyang Yiwei Decoction group, the JAK2 inhibitor group, and the STAT3 inhibitor group. Healthy rats served as the normal control. 24-hour urinary protein excretion, IgG deposition, renal histopathology, the expression levels of synaptopodin, nephrin, podocalyxin, interferon-γ, interleukin- 4, T-box expressed in T cells, GATA binding protein-3, and relevant pathway proteins were measured.

Results: Within the model group, a notable elevation in the 24-h urinary protein level was observed, accompanied by evident IgG deposition, increased glomerular volume, eosinophilic deposits, diminished expression of podocyte marker proteins, and a discernible imbalance in Th1/Th2 cellular immunity. Conversely, in Shengyang Yiwei Decoction and both inhibitor groups, enhancements were observed across the aforementioned indexes.

Conclusion: Shengyang Yiwei Decoction may reduce glomerular podocyte injury through the suppression of the JAK2/STAT3 signaling pathway and modulation of the Th1/Th2 immune balance.

Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article has been withdrawn.

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Bentham science disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article has been withdrawn.

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The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php

Bentham science disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

Shuanghuanglian (SHL) and its primary constituents have demonstrated protective effects against allergenic diseases. This review examines the anaphylactic and anti-allergenic activities of SHL and its constituents. We also discuss potential avenues for future research, particularly regarding the expansion of the clinical applications of SHL formulations (oral or nebulized) for the treatment of allergenic disorders. For this review, we searched the PubMed, Web of Science, and China National Knowledge Infrastructure databases for relevant publications. Additionally, details of the essential active components and target genes of SHL were obtained from the Traditional Chinese Medicine Systems Pharmacology database (TCMSP), and information on allergy-related genes was collected from the GeneCards and Online Mendelian Inheritance in Man(OMIM) databases. Lists of both the SHL target and disease-related genes were imported into the 'Draw Venn Diagram' tool on the website (http://bioinformatics.psb.ugen /web tools/Venn/). A protein-protein interaction network for SHL and disease targets was constructed with reference to the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database, and the potential pathways were identified based on Kyoto Encyclopaedia of Genes and Genome enrichment analyses. The allergenic reactions induced by SHL injection (intravenous) and its main constituents (intraperitoneal or intravenous injection) have been verified in animal experiments. Furthermore, the protective effects of SHL injection (intraperitoneal) and its individual Chinese herb components (intragastric administration), namely, Flos Lonicerae, Radix Scutellariae, and Fructus Forsythiae, as well as their main constituents (intraperitoneal or intragastric administration), have been verified in asthma, rhinitis, atopic dermatitis, and both IgE- and non-IgE-mediated systemic allergic responses. The network pharmacology analysis revealed that the therapeutic effects of SHL might be primarily mediated through the regulation of the IL-17 and TNF-α signalling pathways and Th17 cell differentiation. Accumulated research data provide a theoretical basis for the clinical application of SHL (via extravascular routes) in the treatment of allergenic diseases.

Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article has been withdrawn.

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The Bentham Editorial Policy on Article Withdrawal can be found at https://benthamscience.com/editorial-policies-main.php

Bentham science disclaimer: It is a condition of publication that manuscripts submitted to this journal have not been published and will not be simultaneously submitted or published elsewhere. Furthermore, any data, illustration, structure or table that has been published elsewhere must be reported, and copyright permission for reproduction must be obtained. Plagiarism is strictly forbidden, and by submitting the article for publication the authors agree that the publishers have the legal right to take appropriate action against the authors, if plagiarism or fabricated information is discovered. By submitting a manuscript the authors agree that the copyright of their article is transferred to the publishers if and when the article is accepted for publication.

Background: TSPOAP1 antisense RNA 1 (TSPOAP1-AS1) is a long non-coding RNA (lncRNA) that has received widespread attention in oncology research in recent years. Its role and mechanism in some cancers have gradually been revealed. However, it is not clear what role TSPOAP1-AS1 plays in cervical cancer (CESC).

Objective: In this study, bioinformatic analysis and experimental validation were carried out to investigate the relationship between TSPOAP1-AS1 and CESC.

Methods: The relationships between clinical characteristics in patients with CESC, TSPOAP1-AS1 expression, prognostic factors, regulation network, and immune infiltration of TSPOAP1-AS1 were evaluated using statistics and The Cancer Genome Atlas database. Real-Time Quantitative Reverse Transcription PCR was used to test TSPOAP1-AS1, miR-17-5p, and AGFG2 expression in CESC cell lines.

Results: CESC patients exhibited markedly reduced expression of TSPOAP1-AS1. There was a significant correlation between low expression of TSPOAP1-AS1 in CESC patients and the clinical stage (p < 0.05), weight (p < 0.05), and BMI (p < 0.05). Lower expression of TSPOAP1-AS1 in patients with CESC was associated with poorer overall survival (OS) (p = 0.014) and disease-specific survival (DSS) (p = 0.030). There was also an independent correlation between high expression of TSPOAP1- AS1 (p = 0.036) and DSS in patients with CESC. TSPOAP1-AS1 was involved in the ribosome, oxidative phosphorylation, antigen processing and presentation, cell adhesion molecules (CAMs), the chemokine signaling pathway, neuroactive ligand-receptor interaction, and primary immunodeficiencies. The infiltration of immune cells and the expression of TSPOAP1-AS1 were found to be correlated. A ceRNA network of TSPOAP1-AS1/miR-17-5p/AGFG2 was constructed in CESC. In CESC, a ceRNA network involving TSPOAP1-AS1/miR-17-5p/AGFG2 was successfully established. When comparing CESC cell lines with HcerEpic, the expression of TSPOAP1-AS1 and AGFG2 decreased significantly, and the expression of miR-17-5p increased significantly.

Conclusion: In CESC patients, low expression of TSPOAP1-AS1 was associated with poor survival and immune infiltration. It may be effective to use TSPOAP1-AS1 as a biomarker of prognosis and therapeutic target in CESC.