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PubMed2006

Evidence that miRNAs are different from other RNAs.

An examination of 513 known pre-miRNAs and 237 other RNAs (tRNA, rRNA, and mRNA) revealed that miRNAs were significantly different from other RNAs (p < 0.001). miRNA genes were less conserved than other RNA genes, although their mature miRNA sequences were highly conserved. The A+U content of pre-miRNAs was higher than non-coding RNA (p < 0.001), but lower than mRNAs. The nucleotides in pre-miRNAs formed more hydrogen bonds and base pairs than in other RNAs. miRNAs had higher negative adjusted minimal folding free energies than other RNAs except tRNAs (p < 0.001). The MFE index (MFEI) was a sufficient criterion to distinguish miRNAs from all coding and non-coding RNAs (p < 0.001). The MFEI for miRNAs was 0.97, significantly higher than tRNAs (0.64), rRNAs (0.59), or mRNAs (0.65). Our findings should facilitate the prediction and identification of new miRNAs using computational and experimental strategies.

Base Pairing↗

PubMed2026

The miR-206-3p/Cpeb1 axis delays acetylcholine receptor degradation and preserves neuromuscular junction stability in denervation-induced muscle atrophy.

Peripheral nerve injury leads to progressive neuromuscular junction (NMJ) destabilization and acetylcholine receptor (AChR) degradation, which are critical drivers of denervation-induced muscle atrophy and impaired motor recovery. However, the post-transcriptional mechanisms regulating AChR stability during denervation remain poorly understood. Here, we investigated the role of miR-206-3p in NMJ maintenance and muscle preservation after denervation, with a focus on its interaction with the RNA-binding protein cytoplasmic polyadenylation element binding protein 1 (Cpeb1). Using C2C12 myoblasts and a sciatic nerve transection mouse model, we demonstrate that miR-206-3p promotes myogenic differentiation, enhances AChR clustering, and preserves postsynaptic AChR morphology. miR-206-3p directly targets the 3' untranslated region of Cpeb1, suppressing its expression, as confirmed by dual-luciferase reporter assays. In vivo, adeno-associated virus-mediated overexpression of miR-206-3p delayed denervation-induced AChR fragmentation, attenuated muscle atrophy, and significantly improved motor function recovery. Conversely, Cpeb1 overexpression accelerated AChR degradation and muscle wasting, whereas co-overexpression of miR-206-3p mitigated these detrimental effects, indicating that Cpeb1 is a key downstream effector of miR-206-3p. Collectively, our findings identify the miR-206-3p/Cpeb1 axis as a previously unrecognized regulator of NMJ stability and muscle integrity after denervation, providing mechanistic insight and a potential therapeutic target for preserving neuromuscular function during prolonged denervation.

Animals↗

PubMed2005

Silence of the transcripts: RNA interference in medicine.

Silencing of gene expression by ribonucleic acid (RNA), known as RNA interference (RNAi), is now recognized as a major means of gene regulation in biology. In this mechanism, small noncoding double-stranded RNA molecules knock down gene expression through a variety of mechanisms that include messenger RNA (mRNA) degradation, inhibition of mRNA translation, or chromatin remodeling. The posttranscriptional mechanism of RNAi has been embraced by researchers as a powerful tool for generating deficient phenotypes without mutating the gene. In parallel, exciting recent results have promised its application in disease therapy. This review aims to summarize the current knowledge in this area and provide a roadmap that may eventually launch RNAi from the research bench to the medicine chest.

Animals↗

PubMed2005

RNA interference: ready to silence cancer?

RNA interference (RNAi) is considered the most promising functional genomics tool recently developed. As in other medical fields, this biotechnology might revolutionize the approach to dissecting the biology of cancer, ultimately speeding up the discovery pace of novel targets suitable for molecularly tailored antitumor therapies. In addition, preclinical results suggest that RNAi itself might be used as a therapeutic weapon. With the aim of illustrating not only the potentials but also the current limitations of RNAi as a tool in the fight against cancer, here we summarize the physiology of RNAi, discuss the main technical issues of RNAi-based gene silencing, and review some of the most interesting preclinical results obtained so far with its implementation in the field of oncology.

Animals↗

PubMed2026

Long non-coding RNAs link DNA methylation to immune regulatory networks in bovine subclinical mastitis.

Long non-coding RNAs (lncRNAs) are emerging as important regulators of inflammatory and immune signaling, yet their contribution to bovine subclinical mastitis remains poorly defined. Here, we characterized the lncRNA expression landscape associated with disease in milk somatic cells of healthy and subclinical mastitic Vrindavani cattle. We identified 11,403 high-confidence lncRNAs, of which 104 were differentially expressed in subclinical mastitis (adjusted P < 0.05; |log2FC| ≥ 1), with the vast majority upregulated in mastitic samples. Predicted cis- and trans-associated target analyses identified 637 non-redundant genes, and KEGG analysis identified 8 significantly enriched cis-associated pathways and 152 significantly enriched trans-associated pathways (adjusted P < 0.05), predominantly enriched for immune and inflammation-related pathways. These findings prioritized a subset of mastitis-associated lncRNAs for subsequent methylation and interaction-network analyses. A subset of these lncRNAs further overlapped differentially methylated regions (DMRs), suggesting a potential association between lncRNA expression changes and DNA methylation alterations. Integration of lncRNA-miRNA and miRNA-mRNA interactions identified lncRNA-miRNA-mRNA interaction networks involving DMR-associated lncRNAs. Among the prioritized candidates, MSTRG.28878.1 showed overlap with a hypomethylated promoter-associated DMR, increased expression, and multiple connections within the predicted interaction network. Together, these findings identify candidate lncRNAs, methylation-associated loci, and predicted molecular interactions associated with bovine subclinical mastitis and provide a resource for future functional investigation of candidate non-coding RNA-associated mechanisms in disease.

Animals↗

PubMed2006

miRNA and Dicer in the mammalian lens: expression of brain-specific miRNAs in the lens.

Micro RNAs (miRNAs) are approximately 22 nucleotide molecules that regulate gene expression post-transcriptionally and govern a wide range of physiological and developmental processes. Evidence now indicates that miRNAs can also coordinately down-regulate transcript levels for very large groups of genes in a tissue-specific manner, in addition to their ability to suppress protein translation. Here, we examine expression of specific miRNAs and Dicer ribonuclease that is required for miRNA biogenesis in mouse and rat lenses. Northern blot analysis demonstrated lens expression of brain-specific miR-124 and miR-7 in lenses, as well as miR-125b and let-7a. In addition, we provide evidence that muscle specific miR-1 is not present in lens. We detected Dicer transcripts in 21 day, 6 week, and 1 year mouse lenses and 15 day rat lens, and detected Dicer protein in adult lens protein samples. Immunohistochemical examination of late embryonic, post-natal, and adult rat lens sections identified expression of Dicer in differentiating fiber cells that undergo pronounced cell elongation in the lens interior and anterior epithelial cells. The present study provides evidence that miRNAs, which include brain-specific forms, and Dicer are expressed in mammalian lenses, indicating that fundamental aspects of miRNA biology are utilized by the lens during late embryonic and post-natal development and in adult lenses.

Aging↗

PubMed2026

Circular RNAs orchestrate integrated post-transcriptional responses to combined heat and drought stress in rice.

Circular RNAs (circRNAs) are emerging post-transcriptional regulators, yet their landscape and functional roles in rice under combined abiotic stress remain largely unexplored. Here, we systematically reanalyzed strand-specific RNA-seq data to characterize circRNAs responsive to simultaneous heat and drought stress. Following quality control, read mapping, and dual-algorithm prediction using CIRI2 and CIRCexplorer2, we identified 208 high-confidence circRNAs distributed across all 12 chromosomes. Comparative profiling revealed 83 circRNAs uniquely expressed in control samples, 51 in stressed samples, and 74 shared between conditions, indicating stress-dependent circularization. Junction-read analysis highlighted a spectrum of circularization strength, ranging from highly abundant circRNAs with dominant junction reads to low-confidence candidates masked by linear transcript background. Genomic annotation showed that circRNAs primarily originated from exonic and intergenic regions, with a pronounced negative-strand bias; several genes generated multiple circRNA isoforms via alternative back-splicing. Functional enrichment of host genes suggested involvement in protein folding, nutrient reservoir activity, RNA degradation, and branched-chain amino acid catabolism, implicating roles in stress adaptation and metabolic regulation. Differential expression analysis identified seven circRNAs specifically induced under combined stress conditions. Network topology analysis pinpointed key miRNAs-including osa-miR414, osa-miR1439, and osa-miR2919-as candidate topological hubs within the predicted network. Their predicted target genes, such as those encoding stress-responsive transcription factors and signaling proteins, suggest potential roles in coordinating post-transcriptional responses to combined stress. Network topology analysis pinpointed key miRNAs-including osa-miR414, osa-miR1439, and osa-miR2919-as candidate topological hubs within the predicted network. Their predicted target genes, such as those encoding stress-responsive transcription factors and signaling proteins, suggest potential roles in coordinating post-transcriptional responses to combined stress. Overall, this study provides a comprehensive map of circRNAs in rice under combined heat and drought stress, suggests their potential as ceRNAs based on predictive analysis, and lays a foundation for future experimental validation of circRNA-mediated regulation.

Oryza↗

PubMed2004

Looking through genomics: concepts and technologies for plant and animal genomics.

Explore the source record for details and available documents.

Animals↗

PubMed2025

Targeting FOXK2 in triple-negative breast cancer: Role of the P53/MCAS1/miR-211-5p regulatory axis.

Forkhead box K2 (FOXK2) is over-expressed in several human malignancies, yet how it is regulated triple-negative breast cancer (TNBC) remained unclear. We aimed to clarify whether FOXK2 drives TNBC progression, and elucidate the upstream molecular circuitry that controls FOXK2 abundance. FOXK2 mRNA and protein were quantified by qPCR and Western blot in 30 paired TNBC and adjacent tissues. Some assays assessed proliferation, migration and invasion after FOXK2 knockdown or overexpression. Bioinformatics predicted miR-211-5p targeting FOXK2 and lncRNA MCM3AP-AS1 (MCAS1) targeting miR-211-5p. RNA immunoprecipitation (RIP) and dual-luciferase assays validated these interactions. RNA pulldown, mass spectrometry and ChIP identified p53 binding to the MCAS1 promoter. FOXK2 was upregulated in TNBC tissues as opposed to the para-carcinoma tissues. FOXK2 silencing significantly reduced proliferation, migration and invasion, whereas overexpression accelerated these phenotypes. Mechanistically, MCAS1 acts as a sponge for miR-211-5p, ultimately protecting its target gene FOXK2 from degradation. Furthermore, employing RNA pulldown, mass spectrometry, ChIP, and luciferase reporter assays, our studies revealed a direct interaction between P53 and the promoter of MCAS1. This interaction resulted in the suppression of MCAS1 transcription. Clinical samples from TNBC patients further confirmed a correlation between FOXK2 expression and tumor size, lymphatic involvement, as well as the expression level of Ki-67. Our findings unveil a novel P53/MCAS1/miR-211-5p/FOXK2 regulatory axis that dictates TNBC aggressiveness. FOXK2 may sever as both a prognostic biomarker and a therapeutic target in TNBC.

Humans↗

PubMed2026

Context-dependent effects of MIR100HG on tumorigenic phenotypes and p38/MAPK-AKT signaling in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related mortality worldwide and is characterized by a hypoxic tumor microenvironment that promotes tumor progression, cellular adaptation, and therapeutic resistance. Increasing evidence indicates that long non-coding RNAs (lncRNAs) play critical roles in regulating tumor-associated signaling networks; however, the contribution of MIR100HG to hepatocellular carcinoma progression, particularly under hypoxic conditions, remains insufficiently understood. In this study, we investigated the expression pattern and functional significance of MIR100HG in hepatocellular carcinoma using epithelial-like Hep3B and mesenchymal-like SNU-398 cells, together with non-tumor hepatocytes (Clone-9). Gain- and loss-of-function approaches were employed to evaluate the impact of MIR100HG on tumor-associated cellular phenotypes under both normoxic and hypoxic conditions. Functional assays demonstrated that MIR100HG overexpression significantly enhanced cell proliferation, clonogenic potential, migration, and invasion, whereas MIR100HG silencing markedly suppressed these tumorigenic properties and increased apoptotic cell death. Mechanistic analyses revealed that MIR100HG promotes oncogenic signaling through the p38/MAPK and AKT pathways under normoxic conditions, whereas MIR100HG depletion reduced the phosphorylation of these key signaling proteins. Notably, additional pathway analyses under hypoxia-mimicking conditions revealed a distinct signaling response, in which the MIR100HG-associated activation of p38/MAPK and AKT observed under normoxia was not maintained. Moreover, the expression patterns of AKT-associated regulatory genes, including GAS6 and PTEN, were reversed under hypoxia-mimicking conditions. These findings suggest that the effects of MIR100HG on oncogenic signaling are highly dependent on the cellular oxygenation context and that hypoxia reshapes the downstream signaling consequences of MIR100HG expression in HCC cells. Collectively, our findings identify MIR100HG as a hypoxia-associated oncogenic regulator that enhances tumorigenic phenotypes and promotes survival signaling in hepatocellular carcinoma. These results highlight MIR100HG as a potential biomarker and therapeutic target in liver cancer and provide new insights into the molecular mechanisms underlying hypoxia-driven tumor progression.

Humans↗

PubMed2026

LncRNA H19 promotes vascular remodeling by inhibiting MFN2.

Neointimal hyperplasia, featuring excessive proliferation and migration of vascular smooth muscle cells (VSMCs), is crucial in vascular remodeling diseases. Long non-coding RNA (lncRNA) H19 promotes vascular remodeling, yet underlying mechanisms remain incompletely elucidated. Here, we investigated whether H19 acts via its derivative miR-675-5p. Bioinformatics found a conserved H19/miR-675-5p/MFN2 (mitofusin 2) axis. Cell assays were performed to evaluate the effects of H19 and miR-675-5p on VSMC proliferation and migration. The dual-luciferase reporter gene assay was used to assess the interaction between miR-675-5p and Mfn2 mRNA. The mouse model of common carotid artery ligation was used to evaluate the role of H19 in neointimal hyperplasia. Our data suggested that knockdown of H19 inhibited VSMC proliferation and migration, as well as neointimal hyperplasia. Mechanistically, H19 regulated MFN2 through miR-675-5p, leading to ERK1/2 (extracellular signal-regulated kinase 1/2) activation. In conclusion, we suggest that targeting the H19/miR-675-5p/MFN2/ERK1/2 axis may help to treat vascular remodeling diseases.

Animals↗

PubMed2006

Ultrastructural localization of connexins (Cx36, Cx43, Cx45), glutamate receptors and aquaporin-4 in rodent olfactory mucosa, olfactory nerve and olfactory bulb.

Odorant/receptor binding and initial olfactory information processing occurs in olfactory receptor neurons (ORNs) within the olfactory epithelium. Subsequent information coding involves high-frequency spike synchronization of paired mitral/tufted cell dendrites within olfactory bulb (OB) glomeruli via positive feedback between glutamate receptors and closely-associated gap junctions. With mRNA for connexins Cx36, Cx43 and Cx45 detected within ORN somata and Cx36 and Cx43 proteins reported in ORN somata and axons, abundant gap junctions were proposed to couple ORNs. We used freeze-fracture replica immunogold labeling (FRIL) and confocal immunofluorescence microscopy to examine Cx36, Cx43 and Cx45 protein in gap junctions in olfactory mucosa, olfactory nerve and OB in adult rats and mice and early postnatal rats. In olfactory mucosa, Cx43 was detected in gap junctions between virtually all intrinsic cell types except ORNs and basal cells; whereas Cx45 was restricted to gap junctions in sustentacular cells. ORN axons contained neither gap junctions nor any of the three connexins. In OB, Cx43 was detected in homologous gap junctions between almost all cell types except neurons and oligodendrocytes. Cx36 and, less abundantly, Cx45 were present in neuronal gap junctions, primarily at "mixed" glutamatergic/electrical synapses between presumptive mitral/tufted cell dendrites. Genomic analysis revealed multiple miRNA (micro interfering RNA) binding sequences in 3'-untranslated regions of Cx36, Cx43 and Cx45 genes, consistent with cell-type-specific post-transcriptional regulation of connexin synthesis. Our data confirm absence of gap junctions between ORNs, and support Cx36- and Cx45-containing gap junctions at glutamatergic mixed synapses between mitral/tufted cells as contributing to higher-order information coding within OB glomeruli.

Animals↗

PubMed2006

Cell differentiation and organ initiation at the shoot apical meristem.

Plants continuously generate organs at the flanks of their shoot apical meristems (SAMs). The patterns in which these organs are initiated, also called patterns of phyllotaxis, are highly stereotypic and characteristic for a particular species or developmental stage. This stable, predictable behaviour of the meristem has led to the idea that organ initiation must be based on simple and robust mechanisms. This conclusion is less evident, however, if we consider the very dynamic behaviour of the individual cells. How dynamic cellular events are coordinated and how they are linked to the regular patterns of organ initiation is a major issue in plant developmental biology.

Cell Differentiation↗

PubMed2006

Genetic regulation by non-coding RNAs.

Large scale cDNA sequencing and genome tiling array studies have shown that around 50% of genomic DNA in humans is transcribed, of which 2% is translated into proteins and the remaining 98% is non-coding RNAs (ncRNAs). There is mounting evidence that these ncRNAs play critical roles in regulating DNA structure, RNA expression, protein translation and protein functions through multiple genetic mechanisms, and thus affect normal development of organisms at all levels. Today, we know very little about the regulatory mechanisms and functions of these ncRNAs, which is clearly essential knowledge for understanding the secret of life. To promote this emerging research subject of critical importance, in this paper we review (1) ncRNAs' past and present, (2) regulatory mechanisms and their functions, (3) experimental strategies for identifying novel ncRNAs, (4) experimental strategies for investigating their functions, and (5) methodologies and examples of the application of ncRNAs.

Databases, Nucleic Acid↗

PubMed2005

Genetics and molecular biology of chronic lymphocytic leukemia.

B cell chronic lymphocytic leukemia (CLL) is a clinically heterogeneous disease characterized by accumulation of malignant CD5+ B cells. Multiple molecular events likely contribute to malignant transformation; no single genetic abnormality or event has been shown to be responsible for development of the disease. Significant advances have recently been made towards understanding the genetic and molecular basis for the etiology and clinical course of CLL. Our current understanding is only now bringing us to the point where we can use this information in management and in developing new therapies for patients with CLL. Familial clustering of CLL cases is not uncommon and implicates a genetic basis for the development of the disease in some individuals. Potential interventions in this instance could employ strategies of gene transfer or gene therapy to correct genetic defects or strategies of chemoprevention, none of which is currently under investigation. Greater potential for therapeutic intervention rests with targeting molecular aberrations and altered gene expression in leukemia cells, for example, over expression of the anti-apoptotic proteins of the Bcl-2 family. CLL follows a variable clinical course, with some patients not needing treatment for many years and responding to therapy completely and repeatedly. Other patients have rapidly progressive disease that is refractory to currently available agents and they quickly succumb to their disease. One major recent advance has been the identification of molecular and genetic prognostic factors that can be used in early-stage patients to identify those likely to rapidly progress. This affords the opportunity to tailor management for patients based on the predictable aggressiveness of their disease. Molecular and genetic findings are increasingly influencing management decisions in CLL. Bone marrow transplantation may be considered for a patient with unfavorable prognostic features earlier than for a patient with favorable features and same clinical stage of disease. It is likely that these genetic and molecular-based factors will be targets of new treatment modalities that fundamentally change the management of this disease. In this review we detail the current understanding of the genetics and molecular biology of CLL and introduce potentials for therapeutic intervention.

Biomarkers, Tumor↗

PubMed2026

Genome-Wide Identification and Characterization of Thaumatin-Like Proteins in Potato (Solanum tuberosum L.) and Their Role in Stress Tolerance.

Thaumatin-like proteins (TLPs), part of the Pathogenesis-related protein 5 (PR5) family, play key roles in plant defense against biotic and abiotic stresses. In Solanum tuberosum, a crucial global food crop, the functional diversity of TLPs under stress conditions remains poorly understood, hindering efforts to improve stress tolerance. This study aimed to address this gap by performing a genome-wide identification and characterization of the TLP gene family in potato. We identified 34 TLPs (StTLP1 to StTLP34), distributed across 11 chromosomes. Detailed analyses were conducted on their physicochemical properties, gene structures, conserved motifs, and expression patterns. Promoter analysis revealed multiple stress-responsive cis-elements. Differential expression analysis showed that several StTLPs are significantly regulated in response to salinity, heat, and pathogen infection. Protein-protein interaction and miRNA targeting analyses further highlighted the regulatory networks involving StTLPs in stress adaptation. This study advances the theoretical understanding of the roles of StTLPs in stress response. It provides a valuable genetic resource for future efforts to enhance stress resilience in potato, with potential applications in crop improvement strategies. The 0 l expression of three TLP genes under salt and mannitol stress was verified through real-time PCR analysis after the interval of 15 days. Alterations in the expression patterns of StTLPs offered deeper insight into the involvement of this gene family in diverse abiotic stress responses. All three StTLPs were upregulated under both treatments at 400 mM, relative to their expression at 200 mM. The highest level of upregulation was observed in StTLP20, indicating its prominent role in both stress treatments.

Solanum tuberosum↗

PubMed2006

Somatic stem cells and the origin of cancer.

Most human cancers derive from a single cell targeted by genetic and epigenetic alterations that initiate malignant transformation. Progressively, these early cancer cells give rise to different generations of daughter cells that accumulate additional mutations, acting in concert to drive the full neoplastic phenotype. As we have currently deciphered many of the gene pathways disrupted in cancer, our knowledge about the nature of the normal cells susceptible to transformation upon mutation has remained more elusive. Adult stem cells are those that show long-term replicative potential, together with the capacities of self-renewal and multi-lineage differentiation. These stem cell properties are tightly regulated in normal development, yet their alteration may be a critical issue for tumorigenesis. This concept has arisen from the striking degree of similarity noted between somatic stem cells and cancer cells, including the fundamental abilities to self-renew and differentiate. Given these shared attributes, it has been proposed that cancers are caused by transforming mutations occurring in tissue-specific stem cells. This hypothesis has been functionally supported by the observation that among all cancer cells within a particular tumor, only a minute cell fraction has the exclusive potential to regenerate the entire tumor cell population; these cells with stem-like properties have been termed cancer stem cells. Cancer stem cells can originate from mutation in normal somatic stem cells that deregulate their physiological programs. Alternatively, mutations may target more committed progenitor cells or even mature cells, which become reprogrammed to acquire stem-like functions. In any case, mutated genes should promote expansion of stem/progenitor cells, thus increasing their predisposition to cancer development by expanding self-renewal and pluripotency over their normal tendency towards relative quiescency and proper differentiation.

Animals↗

PubMed2026

Dual Mechanisms Underlie the Repression of Repressor Element 1-Silencing Transcription Factor Expression in Lung Neuroendocrine Carcinoma Cells.

Recent advances in genetic analysis have led to further subtyping of small-cell lung carcinoma (SCLC). The major subtypes of SCLC are the achaete-scute family bHLH transcription factor 1 (ASCL1)-predominant (SCLC-A), neuronal differentiation 1 (NEUROD1)-predominant (SCLC-N), and POU class 2 homeobox 3 (POU2F3) (SCLC-P) subtypes. SCLC-A and SCLC-N tumors express chromogranin A (CHGA) and synaptophysin (SYP), but SCLC-P tumors do not. Large-cell neuroendocrine carcinoma, another type of neuroendocrine carcinoma (NEC), also frequently expresses CHGA and SYP. Because CHGA and SYP expression is controlled by a transrepressor, repressor element 1-silencing transcription factor (REST), the mechanisms underlying REST suppression in NEC were investigated, with a focus on miRNAs and epigenetics, to determine the causes of the differences in the expression of CHGA and SYP between SCLC-A/N and SCLC-P cells. The results showed that miR-375-3p, which was induced by ASCL1 and NEUROD1, repressed REST expression by binding to the 3'-untranslated region of REST mRNA. Bisulfite sequencing and experiments using a DNA methyltransferase inhibitor, a histone deacetylase inhibitor, and chromatin immunoprecipitation-based quantitative PCR revealed that promoter/enhancer hypermethylation and histone deacetylation causes REST gene inactivation in SCLC-A/N. These phenomena were also observed in a large-cell neuroendocrine carcinoma cell line that expressed high levels of ASCL1 and NEUROD1. Taken together, these findings suggest that NEC has dual repressive effects on REST expression, resulting in strict regulation of the expression of CHGA, SYP, and other REST-controlled neuronal/neuroendocrine-specific genes.

Humans↗