MicroRNA (Shariqah, United Arab Emirates)最新文献

Colorectal cancer has become the leading cause of death worldwide, and it is the second most common cancer in women and the third most common cancer in men. Accumulating evidence suggests that genetic and epigenetic factors play a key role in the development of colorectal cancer. Cancer Stem Cells (CSC) play an important role in the suppression or development of cancer in various conditions. In recent years, non-coding RNAs (ncRNA) have been the focus, and the association of CSC and non-coding RNA has played a crucial role in the development of human cancers. These non-coding RNAs are known to be expressed in many cancers. Studies have suggested that ncRNAs are dysregulated in colorectal cancer cells, and different factors, like Wnt and Notch, are involved in this dysregulation. ncRNAs play a significant role in cancer initiation, migration, and resistance to therapies. Moreover, long noncoding RNAs are known to regulate tumor suppressor genes or oncogenes. Targeting different ncRNAs like miRNA, circular RNA, long noncoding RNAs, and small interfering RNA may provide efficient, targeted therapeutic strategies for colon cancer treatment. This review aims to briefly discuss the latest findings on the role of noncoding RNAs in the prognosis and diagnosis of colon cancer.

The revolutionary CRISPR/Cas9 gene editing technology holds immense potential for treating genetic diseases and tackling conditions like cancer. However, efficient delivery remains a significant challenge. This is where nanoparticles come into play, emerging as powerful allies in the realm of drug delivery. Nanoparticles can accommodate larger insertion sizes, enabling the incorporation of larger Cas9 enzymes and complex guide RNAs, thus opening up the possibility of editing previously inaccessible genetic regions. Their relatively straightforward and scalable production processes make them cost-effective options for wider applications. Notably, nanoparticles excel in vivo, demonstrating efficient tissue penetration and targeted delivery, which are crucial for maximizing therapeutic impact while minimizing side effects. This review aims to explore the potential of nanoparticle-based delivery systems for CRISPR/Cas9, highlighting their advantages and challenges in gene editing applications. The diverse range of nanoparticles further bolsters their potential. Polymeric nanoparticles, for instance, offer tunable properties for customization and controlled release of the CRISPR cargo. Lipid-based nanoparticles facilitate efficient cellular uptake and endosomal escape, ensuring the CRISPR components reach the target DNA. Even gold nanoparticles, known for their unique biocompatibility and photothermal properties, hold promise in light-activated editing strategies. Non-viral delivery systems, particularly those based on nanoparticles, stand out due to their inherent advantages. Collectively, the evidence paints a promising picture: nanoparticles are not merely passive carriers but active participants in the CRISPR/Cas9 delivery landscape. Their versatility, efficiency, and safety position them as key enablers of a future where gene editing can revolutionize drug development, offering personalized and targeted therapies for a wide range of diseases.

Introduction: Endometriosis, a prevalent gynecological disorder characterized by the presence of endometrial-like tissue outside the uterus, poses significant challenges in diagnosis and management due to its unclear pathogenesis and lack of specific biomarkers.

Objective: This study investigates the potential use of microRNAs (miRNAs) as key markers in endometriosis by studying two cohorts of patients (14 patients diagnosed with endometriosis and 15 patients with gynecological benign lesions, different from endometriosis).

Methods: MicroRNA sequencing analysis was tested within data management by a custom pipeline designed by Eurofins Genoma Group.

Results: We identified a specific miRNA expression profile associated with endometriosis to feature specific disease molecular clusters to further elucidate the underlying mechanisms driving endometriosis pathogenesis. Data from the present study suggest a specific miRNA scar for endometriosis compared to other gynecological diseases to develop screening tools in early diagnosis and to ameliorate the management of the disease itself.

Conclusion: This study lays the foundation for the identification of key miRNAs involved in the disease pathogenesis to unveil the molecular signatures in the complex scenario of endometriosis. Further validation and exploration of these findings are needed to develop tools to improve molecular diagnosis and to create a machine-learning prediction algorithm in the future.

Introduction: Breast cancer (BC) is the most prevalent cancer among women globally. Metastasis is the leading cause of mortality in most cancers. Early BC detection before metastasis can enhance survival rates. Understanding BC metastasis mechanisms could aid in developing metastasis-specific treatments.

Method: The role of long non-coding RNAs (lncRNA) in cancer progression is recognized, yet the importance of specific lncRNAs in BC, despite potential alterations, remains inadequately explored. We utilized bioinformatics tools to identify novel lncRNAs dysregulated in metastasis. To achieve this objective, the gene expression profile of GSE102484, encompassing metastatic and non-metastatic BC tissue samples, was analyzed using the limma package in R with cut-off criteria set at an adjusted p-value < 0.005 and |fold change (FC)| ≥ 0.5. We used WGCNA analysis to find co-expression genes for lncRNAs. Then, we identified hub genes and performed pathway enrichment to better understand the results. Considering the defined criteria, eight novels of dysregulated lncRNAs and top 10 miRNAs were identified.

Result: Dysregulated lncRNAs are found in yellow, green, brown, purple, and turquoise co-expression modules from WGCNA analysis. Enrichment analysis of these co-expressed modules revealed relevant pathways to metastasis, such as epithelial-to-mesenchymal transition and integrin cell-surface interactions, as well as regulation of HIF1-alpha. In addition, SDPR, TGFB1I1, ILF3, KIF4A, and COL5A1 were identified as hub genes. Based on DElncRNA-miRNADEmRNA connections and co-expression, we ultimately constructed lncRNA-associated ceRNA axes.

Conclusion: The current study may identify novel lncRNAs implicated in BC metastasis; still, additional research is required to determine the potential functions of these lncRNAs in BC metastasis.

Introduction: The differential expression of miRNAs, a key regulator in many cell signaling pathways, has been studied in various malignancies and may have an important role in cancer progression, including colorectal cancer (CRC).

Method: The present study used machine learning and gene interaction study tools to explore the prognostic and diagnostic value of miRNAs in CRC. Integrative analysis of 353 CRC samples and normal tissue data was obtained from the TCGA database and further analyzed by R packages to define the deferentially expressed miRNAs (DEMs). Furthermore, machine learning and Kaplan Meier survival analysis helped better specify the significant prognostic value of miRNAs. A combination of online databases was then used to evaluate the interactions between target genes, their molecular pathways, and the correlation between the DEMs.

Result: The results indicated that miR-19b and miR-20a have a significant prognostic role and are associated with CRC progression. The ROC curve analysis discovered that miR-20a alone and combined with other miRNAs, including hsa-mir-21 and hsa-mir-542, are diagnostic biomarkers in CRC. In addition, 12 genes, including NTRK2, CDC42, EGFR, AGO2, PRKCA, HSP90AA1, TLR4, IGF1, ESR1, SMAD2, SMAD4, and NEDD4L, were found to be the highest score targets for these miRNAs. Pathway analysis identified the two correlated tyrosine kinase and MAPK signaling pathways with the key interaction genes, i.e., EGFR, CDC42, and HSP90AA1.

Conclusion: To better define the role of these miRNAs, the ceRNA network, including lncRNAs, was also prepared. In conclusion, the combination of R data analysis and machine learning provides a robust approach to resolving complicated interactions between miRNAs and their targets.

Introduction: Curcumin is known as a bioactive component that is found in the rhizomes of Curcuma longa. Curcumin is well known for its chemo-preventive and anticancer properties. However, its anticancer mechanism in colorectal cancer treatment is unclear, and some studies have shown that many microRNAs (miRs) could be potential targets for curcumin in colorectal cancer (CRC) treatment, so there is a need for their integration and clarification.

Methods: We systematically searched international databases, including PubMed, Scopus, and Web of Science, until July 2021 by using some relevant keywords.

Results: The search resulted in 87 papers, among which there were 18 related articles. Curcumin was found to cause the upregulation of miR-497, miR-200c, miR-200b, miR-409-3p, miR-34, miR-126, miR-145, miR-206, miR-491, miR-141, miR-429, miR-101, and miR-15a and the downregulation of miR-21, miR-155, miR-221, miR-222, miR-17-5p, miR-130a, miR-27, and miR-20a.

Conclusion: The present review study suggests that curcumin may be useful as a novel therapeutic agent for CRC by altering the expression level of miRs.

Background: Myasthenia gravis is an autoimmune disease, and 30% of patients with thymoma often have myasthenia gravis. Patients with thymoma-associated MG (TAMG) have many different clinical presentations compared to non-MG thymoma (NMG), yet their gene expression differences remain unclear.

Objective: In this study, we analyzed the Differentially Expressed Genes (DEGs) and analyzed their regulatory microRNAs (miRNAs) in TAMG, which will further clarify the possible pathogenesis of TAMG.

Methods: DEGs were calculated using the RNA-sequencing data of TAMG and NMG downloaded from The Cancer Genome Atlas (TCGA) database. R software was then used to analyze the gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of DEGs, while STRING was applied to build the protein-protein interaction (PPI) network and Cytoscape to identify and visualize the hub genes. Immune infiltration significances of hub genes were also explored by using the TIMER database and TCGA database. Upstream microRNAs (miRNAs) of the hub genes were predicted by online software.

Results: We comparatively analyzed the gene expression differences between TAMG and NMG groups. A total of 977 DEGs were identified between the two groups (|log fold change (FC)| >2, adjusted P value <0.050), with 555 down-regulated genes and 422 up-regulated genes. Five top hub genes (CTNNB1, EGFR, SOX2, ERBB2, and EGF) were recognized in the PPI network. Analysis based on the TIMER and TCGA databases suggested that 5 hub genes were correlated with multiple immune cell infiltrations and immune checkpoint-related markers, such as PDCD1, CTLA-4, and CD274, in TAMG patients. Lastly, 5 miRNAs were identified to have the potential function of regulating the hub gene expression.

Conclusion: Our study identified 5 hub genes (CTNNB1, EGFR, SOX2, ERBB2, and EGF) and their 5 regulatory miRNAs in TAMG, and the hub genes were correlated with multiple immune cell infiltrations and immune checkpoint-related markers. Our findings could help partially clarify the pathophysiology of TAMG, which could be new potential targets for subsequent clinical immunotherapy.

Introduction: MicroRNAs (miRNAs), a distinct category of non-coding RNAs, exert multifaceted regulatory functions in a variety of organisms, including humans, animals, and plants. The inventory of identified miRNAs stands at approximately 60,000 among all species, and 1,926 in Homo sapiens manifest miRNA expression.

Method: Their theranostic role has been explored by researchers over the last few decades, positioning them as prominent therapeutic targets as our understanding of RNA targeting advances. However, the limited availability of experimentally determined miRNA structures has constrained drug discovery efforts relying on virtual screening or computational methods, including machine learning and artificial intelligence.

Results: To address this lacuna, miRVim has been developed, providing a repository of human miRNA structures derived from both two-dimensional (MXFold2, CentroidFold, and RNAFold) and three-dimensional (RNAComposer and 3dRNA) structure prediction algorithms, in addition to experimentally available structures from the RCSB PDB repository. miRVim contains 13,971 predicted secondary structures and 17,045 predicted three-dimensional structures, filling the gap of unavailability of miRNA structure data bank. This database aims to facilitate computational data analysis for drug discovery, opening new avenues for advancing technologies, such as machine learning-based predictions in the field of RNA biology.

Conclusion: The publicly accessible structures provided by miRVim, available at https://mirna.in/miRVim, offer a valuable resource for the research community, advancing the field of miRNA-related computational analysis and drug discovery.

Introduction/ Objective: Estrogen plays a protective role in vascular health due, in part, to its regulation of endothelial inflammation. However, the mechanism(s) by which estrogen negatively regulates inflammatory signaling pathways is not completely understood. MicroRNAs (miRNAs) are recognized as sensitive and selective regulators of cardiovascular function, inflammation, and disease, yet the effects of 17β-estradiol on the endothelial miRNA profile are largely unknown. The aim of this study was to determine the effect of 17β-estradiol on the expression of inflammation-associated miRNAs in endothelial cells in vitro.

Methods: Human Umbilical Vein Endothelial cells (HUVECs) were treated with media in the absence (control) and presence of 17β-estradiol (100 nM) for 24 hr. Thereafter, endothelial cell release of cytokines (IL-6 and IL-8), the intracellular expression of the central protein inflammatory mediator NF- B, and the levels of inflammatory-associated miRNAs: miR-126, miR-146a, miR-181b, miR-204, and miR-let-7a, were determined.

Results: 17β-estradiol-treated cells released significantly lower levels of IL-6 (47.6±1.5 pg/mL vs 59.3±4.9 pg/mL) and IL-8 (36.3±2.3 pg/mL vs 44.0±2.0 pg/mL). Cellular expression of total NF- B (26.0±2.8 AU vs 21.2±3.1 AU) was not different between groups; however, activated NF- B (Ser536) (12.9±1.7 AU vs 20.2±2.2 AU) was markedly reduced in 17β-estradiol-treated cells as compared to untreated cells. Furthermore, cellular expressions of miR-126 (1.8±0.3 fold), miR-146a (1.7±0.3 fold), miR-181b (2.1±0.4 fold), miR-204 (1.9±0.4 fold), and miR-Let-7a (1.8±0.3 fold) were markedly increased in response to 17β-estradiol treatment.

Conclusion: These data suggest that the anti-inflammatory effect of 17β-estradiol in endothelial cells may be mediated by miRNAs.

microRNAs are a family of small, non-coding RNA molecules that can regulate the translation of messenger RNAs (mRNAs). Numerous miRNAs have been proposed as potential indicators for periodontal disease, and their regulation might serve as a potent means of restricting the disease process. MiRNAs act as important immune system regulators that promote the production of many cytokines, including interferon (IFN), tumour necrosis factor (TNF), and IL-1as well as RANK. Investigations pertaining to the use of specific miRNAs as therapeutic agents are underway. They can influence a variety of regulatory organs and target several genes. Additionally, distinct components of the same expression pathway can be controlled by combining miRNAs and their antagonists. In recent years, many miRNA delivery methods have been created for therapeutic applications. Studies pertaining to the role of miRNAs in periodontal disease pathogenesis may pave the way for the use of miRNAs as biomarkers of periodontal disease. A complete understanding of the role of miRNA in periodontal disease and its mechanism of action can pave the way towards therapeutic strategies that can reduce or even prevent the progression of periodontal diseases.