MicroRNA - Volume 11, Issue 2, 2022

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.

In eukaryotic organisms such as humans, some noncoding single-stranded RNAs (ncRNAs) contribute to regulating the expression of some genes before and after the transcription process, which in turn controls a number of vital physiological processes, including cell proliferation, differentiation, invasion, angiogenesis, and embryonic development. miR-126 is one of these miRNAs expressed exclusively in endothelial cells such as capillaries and vessels involved in controlling angiogenesis. In recent years, the link between miRs such as miR-126 and the pathology of breast cancer has attracted the attention of many researchers. Numerous studies have shown that miR-126 may be able to suppress tumor tissue metastasis or to increase tumor metastasis through complex molecular mechanisms. There is ample clinical evidence that miR-126 can be used as a biomarker to predict and diagnose breast cancer due to the increased or decreased expression of certain genes in breast cancer tissue. In this review, we discuss the association between the growth and metastasis (tumorigenesis) of breast cancer and miR-126, as well as the relationship between current research advances in the prognosis, diagnosis, and treatment of breast cancer and miR-126.

Allergic asthma is a complicated disease that is affected by many factors. Numerous cytokines and signaling pathways are attributed to the cause of asthma symptoms. MicroRNAs (miRNAs) are a group of small non-coding single-stranded RNA molecules that are involved in gene silencing and posttranscriptional regulation of gene expression by targeting mRNAs. In pathological conditions, altered expression of microRNAs differentially regulates cytokines and signaling pathways and therefore, can be the underlying reason for the pathogenesis of allergic asthma. Indeed, microRNAs participate in airway inflammation via inducing airway structural cells and activating immune responses by targeting cytokines and signaling pathways. Thus, to make a complete understanding of allergic asthma, it is necessary to investigate the communication network of microRNAs with cytokines and signaling pathways which is contributed to the pathogenesis of allergic asthma. Here, we shed light on this aspect of asthma pathology by Summarizing our current knowledge of this topic.

MicroRNAs (miRNAs) are small non-coding RNAs that regulate the translation of mRNA and protein, mainly at the posttranscriptional level. Global expression profiling of miRNAs has demonstrated a broad spectrum of aberrations that correlated with several diseases, and miRNA- 10a and miRNA-10b were the first examined miRNAs to be involved in abnormal activities upon dysregulation, including many types of cancers and progressive diseases. It is expected that the same miRNAs behave inconsistently within different types of cancer. This review aims to provide a set of information about our updated understanding of miRNA-10a and miRNA-10b and their clinical significance, molecular targets, current research gaps, and possible future applications of such potent regulators.

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.

Background: Toxoplasma gondii (T. gondii) is an intracellular zoonotic protozoan parasite known to effectively modulate the host system for its survival. A large number of microRNAs (miRNAs) regulated by different strains of T. gondii in diverse types of host cells/tissues/organs have been reported across multiple studies. Objective: We aimed to decipher the complexity of T. gondii regulated spectrum of miRNAs to derive a set of core miRNAs central to different strains of T. gondii infection in diverse human cell lines. Methods: We first assembled miRNAs hat are regulated by T. gondii altered across the various assortment of infections and time points of T. gondii infection in multiple cell types. For these assembled datasets, we employed specific criteria to filter the core miRNAs regulated by T. gondii. Subsequently, accounting for the spectrum of miRNA-mRNA target combinations, we applied a novel confidence criterion to extract their core experimentally-validated mRNA targets in human cell systems. Results: This analysis resulted in the extraction of 74 core differentially regulated miRNAs and their 319 high-confidence mRNA targets. Based on these core miRNA-mRNA pairs, we derived the central biological processes perturbed by T. gondii in diverse human cell systems. Further, our analysis also resulted in the identification of novel autocrine/paracrine signalling factors that could be associated with host response modulated by T. gondii. Conclusion: The current analysis derived a set of core miRNAs, their targets, and associated biological processes fine-tuned by T. gondii for its survival within the invaded cells.