MicroRNA (Shariqah, United Arab Emirates)最新文献

Diagnosis and management of prostatic cancer (PCa) cases mainly rely on levels of prostatic- specific antigen (PSA) levels. In the majority of cases, rising of PCa is usually responsible for elevated PSA. However, a wide variety of prostatic abnormalities, such as benign prostatic hyperplasia and infection or inflammation of the prostatic glands, may also impact prostate levels. Due to the low specificity and sensitivity of the PSA test, elevated PSA levels can lead to unnecessary prostate biopsies or surgical interventions, constituting this diagnostic modality a controversial screening test. Therefore, the discovery of new non-invasive biomarkers, such as urinary miRNAs, could shed light on the optimal management and follow-up of patients with prostatic lesions. This study aims to evaluate the utility of urinary miRNAs as a new PCa prognostic biomarker, discovering its current limitations and proposing methods to overwhelm current challenges.

Different modes of gene regulation, such as histone modification, transcription factor binding, DNA methylation, and microRNA (miRNA) expression, are critical for the spatiotemporal expression of genes in developing orofacial tissues. Aberrant regulation in any of these modes may contribute to orofacial defects. Noncoding RNAs (ncRNAs), such as long ncRNAs (lncRNAs) and circular RNAs (circRNAs), have been shown to alter miRNA expression, and are thus emerging as novel contributors to gene regulation. Some of these appear to function as 'miRNA sponges', thereby diminishing the availability of these miRNAs to inhibit the expression of target genes. Such ncRNAs are also termed competitive endogenous RNAs (ceRNAs). Here, we examine emerging data that shed light on how lncRNAs and circRNAs may alter miRNA regulation, thus affecting orofacial development and potentially contributing to orofacial clefting.

Since the authors are not responding to the editor’s requests to fulfill the editorial requirement, therefore, the article hasbeen withdrawn.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-policiesmain.php

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

Background: MicroRNAs (miRNAs) have a pivotal role in Hepatitis B Virus (HBV) infection and its complications by targeting the cellular transcription factors required for gene expression or directly binding to HBV transcripts. Single Nucleotide Polymorphisms (SNPs) in miRNA genes affect their expression and the regulation of target genes, clinical course, diagnosis, and therapeutic interventions of HBV infection.

Methods: Computational assessment and cataloging of miRNA gene polymorphisms targeting mRNA transcripts straightly or indirectly through the regulation of hepatitis B infection by annotating the functional impact of SNPs on mRNA-miRNA and miRNA-RBS (miRNA binding sites) interaction were screened by applying various universally available datasets such as the miRNA SNP3.0 software.

Results: 2987 SNPs were detected in 139 miRNAs affecting hepatitis B infection. Among them, 313 SNPs were predicted to have a significant role in the progression of hepatitis B infection. The computational analysis also revealed that 45 out of the 313 SNPs were located in the seed region and were more important than others. Has-miR-139-3p had the largest number of SNPs in the seed region (n=6). On the other hand, proteoglycans in cancer, adherens junction, lysine degradation, NFkappa B signaling cascade, ECM-receptor binding, viral carcinogenesis, fatty acid metabolism, TGF-beta signaling pathway, p53 signaling pathway, immune evasion related pathways, and fatty acid biosynthesis were the most important pathways affected by these 139 miRNAs.

Conclusion: The results revealed 45 SNPs in the seed region of 25 miRNAs as the catalog in miRNA genes that regulated the hepatitis B infection. The results also showed the most important pathways regulated by these miRNAs that can be targeted for therapeutic purposes.

It is well recognized that diet components are important genomic regulators considering that food intake influences cytokines such as leptin, ghrelin, adiponectin, and NPY, which regulate gene expression in response to different nutritional programs, particularly regarding the caloric balance. However, the single nutrients, both the macro-nutrients, the fatty acids, and above all the micronutrients, show an essential capacity also for epigenetic regulation; in this sense, vitamins and their derivatives polyphenols are the main actors.

Background: Since ancient times, "betel leaf" (Piper betle) has been revered for its religious, cultural, and medicinal properties. Phytochemicals from the Piper betle are effective in a variety of conditions, including cancer. To date, however, no genomic study or evidence has been found to elucidate the regulatory mechanism that underpins its therapeutic properties. This is the first study of its kind to predict Piper betle miRNAs and also the first genomics source representation of Piper betle. According to previous research, miRNAs from the plants we eat can regulate gene expression. In line with this, our in-silico study revealed that Piper betle and human cross-kingdom control occurs.

Methods: This study demonstrates the prediction and in-silico validation of Piper betle miRNAs from NGS-derived transcript sequences. The cross-kingdom regulation, which can also be understood as inter- species RNA regulation, was studied to identify human mRNA targets controlled by Piper betle miRNAs. Functional annotation and gene-disease association of human targets were performed to understand the role of Piper betle miRNAs in human health and disease. The protein-protein interaction and expression study of targets was further carried out to decipher their role in cancer development.

Results: Identified six Piper betle miRNAs belonging to miR156, miR164, miR172, and miR535 families were discovered to target 198 human mRNAs involved in various metabolic and disease processes. Angiogenesis and the cell surface signaling pathway were the most enriched gene ontology correlated with targets, both of which play a critical role in disease mechanisms, especially in the case of carcinoma. In an analysis of gene-disease interactions, 40 genes were found to be related to cancer. According to a protein-protein interaction, the CDK6 gene, which is thought to be a central regulator of cell cycle progression, was found as a hub protein, affecting the roles of CBFB, SAMD9, MDM4, AXIN2, and NOTCH2 oncogenes. Further investigation revealed that pbe-miRNA164a can be used as a regulator to minimise disease severity in Acute Myeloid Leukemia, where CDK6 expression is highest compared to normal cells.

Conclusion: The predicted pbe-miRNA164a in this study can be a promising suppressor of CDK6 gene involved in tumour angiogenesis. In vivo validation of the pbe-miRNA164a mimic could pave the way for new opportunities to fight cancer and leverage the potential of Piper betle in the healthcare sector.

Background: Hematologic malignancies are among fatal diseases with different subtypes. Acute myeloid leukemia (AML) is a subtype showing a high invasion rate to different tissues.

Objective: AML patients, even after treatment, show an increased rate of recurrence, and this relapsed profile of AML has turned this malignancy into big challenges in the medical scope.

Methods: In the current study, we aimed to investigate hub-genes and potential signaling pathways in AML recurrence. Two expression profiles of genes and non-coding RNAs were extracted from the Gene Expression Omnibus (GEO) database. Target genes of identified miRNAs were predicted through bioinformatics tools. GO and KEGG pathway enrichment analyses were conducted to discover common target genes and differentially expressed genes. Protein-protein interaction (PPI) network was constructed and visualized through the STRING online database and Cytoscape software, respectively. Hub-genes of constructed PPI were found through the CytoHubba plugin of Cytoscape software.

Results: As a result, 109 differentially expressed genes and 45 differentially expressed miRNAs were found, and the top enriched pathways were immune response, xhemokine activity, immune System, and plasma membrane. The hub-genes were TNF, IL6, TLR4, VEGFA, PTPRC, TLR7, TLR1, CD44, CASP1, and CD68.

Conclusion: The present investigation based on the in silico analysis and microarray GEO databases may provide a novel understanding of the mechanisms related to AML relapse.