Role Of lncRNAs Research Articles

Long non-coding RNA involved in the carcinogenesis of human female cancer-a comprehensive review.

Recent years have seen an increase in our understanding of lncRNA and their role in various disease states. lncRNA molecules have been shown to contribute to carcinogenesis and influence the various cancer hallmarks and signalling pathways. It is pertinent to understand the specific contributions and mechanisms of action of these molecules in various cancers. This review provides an overview of the various lncRNA entities that influence and regulate the gynaecological cancers, namely, cervical, breast, ovarian and uterine cancers. The review curates a list of the key players and their effect on cellular processes. lncRNA molecules show immense potential to be used as diagnostic and prognostic indicators and in therapeutic strategies. Several phytochemicals, small molecules, RNA-based regulators, oligos and gene editing tools show promise as a therapeutic strategy. While this review highlights the promising developments in this field, it also underscores the necessity for further research to delineate the complex role of lncRNAs in cancer.

Long Non-Coding RNAs: Crucial Regulators in Alzheimer's Disease Pathogenesis and Prospects for Precision Medicine.

Long non-coding RNAs (LncRNAs) have emerged as pivotal regulators in the pathogenesis of Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by cognitive decline and memory loss. With the capacity to modulate gene expression at various levels, LncRNAs are implicated in multiple pathological mechanisms of AD, including amyloid-beta (Aβ) accumulation, tau protein phosphorylation, neuroinflammation, and neuronal apoptosis. Recent studies have highlighted the potential of LncRNAs as diagnostic biomarkers and therapeutic targets due to their differential expression patterns in AD patients. This review synthesizes current knowledge on the role of LncRNAs in AD, focusing on their involvement in key molecular pathways and their promise as indicators for early diagnosis and prognosis. We discuss the regulatory networks of LncRNAs in the context of AD, their interaction with miRNAs, and the implications for developing novel therapeutic strategies. Despite the complexity and variability in LncRNA function, the prospect of harnessing these molecules for precision medicine in AD is gaining momentum. The translational potential of LncRNA-based interventions offers a new frontier in the quest for effective treatments and a deeper understanding of the molecular underpinnings of AD.

STAT3-related lncRNAs in colorectal cancer progression; Special focus on immune cell's evasion.

Colorectal cancer (CRC) is globally ranked as the third leading cause of cancer-related deaths in both men and women. There is an urgent need for novel biomarkers to facilitate early diagnosis and enhance patient care, thereby improving treatment response and reducing mortality rates. Signal transducer and activator of transcription 3 (STAT3) is essential for controlling the anti-tumor immune response since it is a hub for several oncogenic signaling pathways. In the tumor environment, STAT3 is widely overactivated in both malignant and non-cancerous cells. It is involved in suppressing the expression of critical immune activation regulators and encouraging the synthesis of immunosuppressive substances. Long noncoding RNAs (lncRNAs), a kind of non-coding RNA, are critical for CRC development, apoptosis, and metastasis because they influence important signaling pathways such as STAT3 signaling and contribute to gene regulation at the epigenetic, transcriptional, and post-transcriptional levels. Moreover, lncRNAs have a significant role in modifying the TME and control the expression of important immunological checkpoints, such as PD-L1. Therefore, a comprehensive understanding of the regulatory roles of lncRNAs is crucial for identifying diagnostic, prognostic, and predictive biomarkers for CRC. Thus, the objective of the present review study is to provide a comprehensive overview of the interaction between the STAT3 signaling pathway and various lncRNAs, as well as their implications for apoptosis, metastasis, and immune evasion in CRC.

Long Non-Coding RNAs in Ovarian Cancer: Mechanistic Insights and Clinical Applications

Background/Objectives: Ovarian cancer is a leading cause of gynecological cancer mortality worldwide, often diagnosed at advanced stages due to vague symptoms and the lack of effective early detection methods. Long non-coding RNAs (lncRNAs) have emerged as key regulators in cancer biology, influencing cellular processes such as proliferation, apoptosis, and chemoresistance. This review explores the multifaceted roles of lncRNAs in ovarian cancer pathogenesis and their potential as biomarkers and therapeutic targets. Methods: A comprehensive literature review was conducted to analyze the structural and functional characteristics of lncRNAs and their contributions to ovarian cancer biology. This includes their regulatory mechanisms, interactions with signaling pathways, and implications for therapeutic resistance. Advanced bioinformatics and omics approaches were also evaluated for their potential in lncRNA research. Results: The review highlights the dual role of lncRNAs as oncogenes and tumor suppressors, modulating processes such as cell proliferation, invasion, and angiogenesis. Specific lncRNAs, such as HOTAIR and GAS5, demonstrate significant potential as diagnostic biomarkers and therapeutic targets. Emerging technologies, such as single-cell sequencing, provide valuable insights into the tumor microenvironment and the heterogeneity of lncRNA expression. Conclusions: LncRNAs hold transformative potential in advancing ovarian cancer diagnosis, prognosis, and treatment. Targeting lncRNAs or their associated pathways offers promising strategies to overcome therapy resistance and enhance personalized medicine. Continued research integrating omics and bioinformatics will be essential to unlock the full clinical potential of lncRNAs in ovarian cancer management.

Global identification and regulatory network analysis reveal the significant roles of lncRNAs during anther and pollen development in Arabidopsis.

A high-throughput sequencing identified 1283 lncRNAs in anthers at different stages in Arabidopsis and their relationship with protein-coding genes and miRNAs during anther and pollen development were analyzed. Long non-coding RNAs (lncRNAs) are important regulatory molecules involved in various biological processes. However, their roles in male reproductive development and interactions with miRNAs remained elusive. In this study, a high-throughput sequencing of anthers at different developmental stages in Arabidopsis identified 1283 lncRNAs including 524 differentially expressed lncRNAs (DELs). Most of these DELs exhibited positive correlations with the expression patterns of adjacent protein-coding genes. Weighted gene co-expression network analysis (WGCNA) revealed that protein-coding genes targeted by DELs in four modules related to the tetrad stage were associated with functions such as pollen wall formation, pollen germination, or pollen tube growth, respectively. Furthermore, five, 10, and 11 lncRNAs were predicted as miRNAs' endogenous target mimics (eTMs), precursors, and natural antisense transcripts of pri-miRNA, respectively. Remarkably, the lncRNA, host gene of ath-miR167a (ath-miR167aHG), predicted as the precursor of miR167a, was selected for function validation. Its overexpression resulted in the up-regulation of miR167a and the subsequent down-regulation of miR167a's target genes ARF6 and ARF8, demonstrating a functional interaction between ath-miR167aHG and miR167a. The transgenic plants showed delayed flowering, shorter filaments, abnormal anther dehiscence, and undeveloped siliques ultimately, suggesting a role of ath-miR167aHG in male reproductive development. Collectively, our research shed new light on the functions of lncRNAs in male reproductive development and uncovered the unique interactions between lncRNAs and miRNAs.

The Relationship Between Differential Expression of Non-coding RNAs (TP53TG1, LINC00342, MALAT1, DNM3OS, miR-126-3p, miR-200a-3p, miR-18a-5p) and Protein-Coding Genes (PTEN, FOXO3) and Risk of Idiopathic Pulmonary Fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a rapidly progressive interstitial lung disease of unknown pathogenesis with no effective treatment currently available. Given the regulatory roles of lncRNAs (TP53TG1, LINC00342, H19, MALAT1, DNM3OS, MEG3), miRNAs (miR-218-5p, miR-126-3p, miR-200a-3p, miR-18a-5p, miR-29a-3p), and their target protein-coding genes (PTEN, TGFB2, FOXO3, KEAP1) in the TGF-β/SMAD3, Wnt/β-catenin, focal adhesion, and PI3K/AKTsignaling pathways, we investigated the expression levels of selected genes in peripheral blood mononuclear cells (PBMCs) and lung tissue from patients with IPF. Lung tissue and blood samples were collected from 33 newly diagnosed, treatment-naive patients and 70 healthy controls. Gene expression levels were analyzed by RT-qPCR. TaqMan assays and TaqMan MicroRNA assay were employed to quantify the expression of target lncRNAs, mRNAs, and miRNAs. Our study identified significant differential expression in PBMCs from IPF patients compared to healthy controls, including lncRNAs MALAT1 (Fold Change = 3.809, P = 0.0001), TP53TG1 (Fold Change = 0.4261, P = 0.0021), and LINC00342 (Fold Change = 1.837, P = 0.0448); miRNAs miR-126-3p (Fold Change = 0.102, P = 0.0028), miR-200a-3p (Fold Change = 0.442, P = 0.0055), and miR-18a-5p (Fold Change = 0.154, P = 0.0034); and mRNAs FOXO3 (Fold Change = 4.604, P = 0.0032) and PTEN (Fold Change = 2.22, P = 0.0011). In lung tissue from IPF patients, significant expression changes were observed in TP53TG1 (Fold Change = 0.2091, P = 0.0305) and DNM3OS (Fold Change = 4.759, P = 0.05). Combined analysis of PBMCs expression levels for TP53TG1, MALAT1, miRNA miR-126-3p, and PTEN distinguished IPF patients from healthy controls with an AUC = 0.971, sensitivity = 0.80, and specificity = 0.955 (P = 6 × 10-8). These findings suggest a potential involvement of the identified ncRNAs and mRNAs in IPF pathogenesis. However, additional functional validation studies are needed to elucidate the precise molecular mechanisms by which these lncRNAs, miRNAs, and their targets contribute to PF.

Organoid modeling identifies USP3-AS1 as a novel promoter in colorectal cancer liver metastasis through increasing glucose-driven histone lactylation.

Dysregulation of long non-coding RNAs (lncRNAs) is common in colorectal cancer liver metastasis (CRLM). Emerging evidence links lncRNAs to multiple stages of metastasis from initial migration to colonization of distant organs. In this study we investigated the role of lncRNAs in metabolic reprogramming during CRLM using patient-derived organoid (PDO) models. We established five pairs of PDOs from primary tumors and matched liver metastatic lesions, followed by microarray analysis. We found that USP3-AS1 was significantly upregulated in CRLM-derived PDOs compared to primary tumors. High level of USP3-AS1 was positively associated with postoperative liver metastasis and negatively correlated with the prognosis of colorectal cancer (CRC) patients. Overexpression of USP3-AS1 significantly enhanced both sphere formation efficiency and liver metastasis in PDOs. Gene set enrichment analysis revealed that USP3-AS1 upregulation significantly enriched glycolysis and MYC signaling pathways. Metabolomics analysis confirmed that USP3-AS1 promoted glycolysis in PDOs, whereas glycolysis inhibition partially attenuated the effects of USP3-AS1 overexpression on PDO growth and liver metastasis. We revealed that USP3-AS1 stabilized MYC via post-translational deubiquitination, thereby promoting glycolysis. We demonstrated that USP3-AS1 increased the stability of USP3 mRNA, resulting in higher USP3 protein expression. The elevated USP3 protein then interacted with MYC and promoted its stability by deubiquitination. The USP3-AS1-MYC-glycolysis regulatory axis modulated liver metastasis by promoting H3K18 lactylation and CDC27 expression in CRC. In conclusion, USP3-AS1 is a novel promoter of CRLM by inducing histone lactylation.

Nonylphenol exposure increases the risk of Hirschsprung's disease by inducing macrophage M1 polarization.

Nonylphenol (NP), a ubiquitous environmental contaminant used as a surfactant in industrial production and classified as an endocrine disruptor, could interfere hormone secretion and exhibit neurotoxicity in organisms. Hirschsprung's disease (HSCR), one of the most frequently observed congenital malformations of the digestive system, arises mainly due to the failure of enteric neural crest cells to migrate to the distal colon during embryonic development. However, the effects of NP exposure on HSCR are largely unknown. Herein, we identified the content of NP and expression of lncRNA LINC00294/Inhibin Subunit Beta E (INHBE) axis in clinical samples and evaluated the crucial role of lncRNA LINC00294/INHBE axis in the neurogenic potential of neurons and the neurotoxicity effects of NP in the SH-SY5Y cells and female specific pathogen-free (SPF) rat model. Our results showed that NP concentration and LINC00294 were significantly associated with HSCR occurrence and macrophage polarization in human HSCR specimens. Moreover, NP promoted macrophage M1 polarization. The proliferation and migration were weakened, and apoptosis was heightened by the conditioned medium of NP-treated macrophages in SH-SY5Y cells. Contrarily, LINC00294 overexpression and INHBE knockdown reversed the neurotoxicity effect of NP on SH-SY5Y cells. Furthermore, the neurotoxicity effect of NP was abolished by clodronate liposomes in the rat model. In conclusion, NP could induce macrophage M1 polarization via the LINC00294/INHBE axis and increase the risk of Hirschsprung's disease. Our findings would provide a foundation for the toxicity study and risk assessments of NP.

The role of lncRNAs in the interplay of signaling pathways and epigenetic mechanisms in glioma.

Gliomas, highly aggressive tumors of the central nervous system, present overwhelming challenges due to their heterogeneity and therapeutic resistance. Glioblastoma multiforme (GBM), the most malignant form, underscores this clinical urgency due to dismal prognosis despite aggressive treatment regimens. Recent advances in cancer research revealed signaling pathways and epigenetic mechanisms that intricately govern glioma progression, offering multifaceted targets for therapeutic intervention. This review explores the dynamic interplay between signaling events and epigenetic regulation in the context of glioma, with a particular focus on the crucial roles played by non-coding RNAs (ncRNAs). Through direct and indirect epigenetic targeting, ncRNAs emerge as key regulators shaping the molecular landscape of glioblastoma across its various stages. By dissecting these intricate regulatory networks, novel and patient-tailored therapeutic strategies could be devised to improve patient outcomes with this devastating disease.

The Role of Long Non-Coding RNA in the Pathogenesis of Psoriasis.

Psoriasis is a chronic immune-mediated disease with complex pathogenesis. The altered proliferation and differentiation of keratinocytes, together with the activity of dendritic cells and T cells, are crucial drivers of psoriasis progression. Long non-coding RNAs (lncRNAs) are composed of over 200 nucleotides and exert a large variety of functions, including the regulation of gene expression. Under pathological conditions, the expression of lncRNAs is frequently dysregulated. Recent studies demonstrated that lncRNAs significantly affect major cellular processes, and their aberrant expression is likely involved in the pathogenesis of various disorders. In this review, we will discuss the role of lncRNAs in the pathophysiology of psoriasis. We will summarize recent studies that investigated the relationships between lncRNAs and keratinocyte proliferation and pro-inflammatory responses.

The Expression Pattern and Functional Analysis of Extracellular Vesicle Long Non-Coding RNAs from Uterine Fluid During Implantation in Pig.

Long non-coding RNAs (lncRNAs) act as competing endogenous RNAs and play significant roles in porcine embryo development. Extracellular vesicles (EVs) in the uterine fluid (UF) can target and deliver maternal endometrial signalling molecules to embryonic trophoblast cells, exerting crucial regulatory effects during embryo implantation. However, the specific roles of lncRNAs carried by UF-EVs during the embryo implantation period have not been thoroughly reported in the literature. In the present study, high-throughput sequencing and biological tools were applied to analyse lncRNAs in UF-EVs on days 9, 12, and 15 of pregnancy to identify key regulatory lncRNAs in UF-EVs during the porcine embryonic implantation period and to explore their expression patterns and functional roles. A total of 30,203 lncRNAs were identified and 7879 differentially expressed lncRNAs were screened, and qRT-PCR was used to verify the sequencing data. Days 9-12 of pregnancy represent a critical stage of embryo implantation characterised by substantial morphological changes in porcine embryos. During this period, we identified a total of 4348 differentially expressed lncRNAs. Through screening and validation, we discovered that LNC_026212 was highly expressed on day 12 of pregnancy and can promote the proliferation and migration of porcine trophoblast cells (PTr cells). These novel findings contribute to our understanding of the impact of lncRNAs on porcine reproductive processes, offering new research directions to improve the success rate of embryo implantation in pigs.

Developing a ceRNA-based lncRNA-miRNA-mRNA regulatory network to uncover roles in skeletal muscle development.

The precise role of lncRNAs in skeletal muscle development and atrophy remain elusive. We conducted a bioinformatic analysis of 26 GEO datasets from mouse studies, encompassing embryonic development, postnatal growth, regeneration, cell proliferation, and differentiation, using R and relevant packages (limma et al.). LncRNA-miRNA relationships were predicted using miRcode and lncBaseV2, with miRNA-mRNA pairs identified via miRcode, miRDB, and Targetscan7. Based on the ceRNA theory, we constructed and visualized the lncRNA-miRNA-mRNA regulatory network using ggalluvial among other R packages. GO, Reactome, KEGG, and GSEA explored interactions in muscle development and regeneration. We identified five candidate lncRNAs (Xist, Gas5, Pvt1, Airn, and Meg3) as potential mediators in these processes and microgravity-induced muscle wasting. Additionally, we created a detailed lncRNA-miRNA-mRNA regulatory network, including interactions such as lncRNA Xist/miR-126/IRS1, lncRNA Xist/miR-486-5p/GAB2, lncRNA Pvt1/miR-148/RAB34, and lncRNA Gas5/miR-455-5p/SOCS3. Significant signaling pathway changes (PI3K/Akt, MAPK, NF-κB, cell cycle, AMPK, Hippo, and cAMP) were observed during muscle development, regeneration, and atrophy. Despite bioinformatics challenges, our research underscores the significant roles of lncRNAs in muscle protein synthesis, degradation, cell proliferation, differentiation, function, and metabolism under both normal and microgravity conditions. This study offers new insights into the molecular mechanisms governing skeletal muscle development and regeneration.

LncRNA 3222401L13Rik Is Upregulated in Aging Astrocytes and Regulates Neuronal Support Function Through Interaction with Npas3.

Aging leads to cognitive decline and increased risk of neurodegenerative diseases. While molecular changes in central nervous system (CNS) cells contribute to this decline, the mechanisms are not fully understood. Long non-coding RNAs (lncRNAs) are key regulators of cellular functions. Background/Objectives: The roles of lncRNAs in aging, especially in glial cells, are not well characterized. Methods: We investigated lncRNA expression in non-neuronal cells from aged mice and identified 3222401L13Rik, a previously unstudied lncRNA, as upregulated in astrocytes during aging. Results: Knockdown of 3222401L13Rik in primary astrocytes revealed its critical role in regulating genes for neuronal support and synapse organization, a function conserved in human iPSC-derived astrocytes. A 3222401L13Rik interacts with the transcription factor Neuronal PAS Domain Protein 3 (Npas3), and overexpression of Npas3 rescues deficits in astrocytes lacking 3222401L13Rik. Conclusions: These data suggest that 3222401L13Rik upregulation may help delay age-related cognitive decline.

Long noncoding RNA FAM111A-DT promotes aggressiveness of papillary thyroid cancer via activating NF-κB signaling.

Long noncoding RNAs (lncRNAs) play crucial regulatory roles in the tumorigenesis and progression of various cancers. However, the functional roles of lncRNAs in papillary thyroid cancer (PTC) remain unclear. In this study, we investigated the functional role of the lncRNA FAM111A-DT in PTC progression and the underlying mechanisms. Different expression levels of lncRNAs in PTC were compared via analysis of the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. Bioinformatics analyses and qRT‒PCR were used to investigate the expression of FAM111A-DT in PTC. Cell proliferation was measured via CCK8, EdU, colony formation, and flow cytometry assays. Cell migration and invasion were examined by wound healing and Transwell assays. Apoptosis was detected via flow cytometry. RNA sequencing, qRT‒PCR, Western blot, immunofluorescence and dual-luciferase reporter assays were performed to assess the underlying mechanisms involved. FAM111A-DT was highly expressed in PTC and associated with poor prognosis, thyroid dedifferentiation, various clinical features and the BRAFV600E mutation in PTC patients. Overexpression of FAM111A-DT enhanced the proliferation, migration and invasion of PTC cells while reducing their degree of apoptosis. The NF-κB signaling pathway was activated in FAM111A-DT-overexpressing PTC cells. The NF-κB inhibitor PDTC attenuated the promotive effects of FAM111A-DT on aggressive phenotypes and NF-κB pathway activity in PTC cells. FAM111A-DT is upregulated in PTC, and its expression is associated with poor clinical outcomes. FAM111A-DT plays an oncogenic role by, at least partially, activating the NF-κB signaling pathway.

Long Non-Coding RNAs in Diabetic Cardiomyopathy: Potential Function as Biomarkers and Therapeutic Targets of Exercise Training.

Recent studies emphasize the beneficial effects of exercise on diabetic cardiomyopathy (DCM), adding to the growing body of evidence that underscores the role of exercise in improving health outcomes. Despite this, a notable gap persists in the number of healthcare providers who actively prescribe exercise as a therapeutic intervention for DCM management. In addition, exercise modulates the expression of lncRNAs, which play a pivotal role in DCM progression. Further investigation into this relationship may facilitate the identification of novel biomarkers and therapeutic targets for DCM. This review consolidates recent advances in identifying lncRNAs biomarkers in DCM, summarizing the current knowledge on dysregulated lncRNAs and their molecular mechanisms. Additionally, it offers new insights into the mechanistic roles of lncRNAs, highlighting their potential as biomarkers and therapeutic targets for DCM. Overall, this review aims to inform future research and reinforce the significance of addressing diabetes-related cardiovascular diseases to potentially improve clinical outcomes.

MtCIR2 negatively regulates seed germination to salt stress by disrupting metabolisms and signaling of abscisic acid and gibberellins.

Emerging evidence indicates that long non-coding RNAs (lncRNAs) play a regulatory role in plant response to environmental stresses. Seed germination is a complex physiological process modulated by many environmental and phytohormonal cues. However, how lncRNAs and phytohormones interactively regulate the response of seed germination to salt stress remain largely unknown. Here, we functionally characterized a salt-responsive lncRNA from legume species Medicago truncatula, referred to as MtCIR2, in response to salt stress during seed germination by heterologously expressing MtCIR2 in Arabidopsis in which none such homologous sequence was detected. Expressing MtCIR2 in Arabidopsis rendered the seed germination more sensitive to salt stress. We further evaluated whether and how abscisic acid (ABA) and gibberellin (GA) were involved in the MtCIR2-mediated seed germination in response to salt stress. We found that expression of MtCIR2 led to an increase in endogenous ABA concentration and a decrease in overall GA concentration due to enhanced expression of ABA catabolic gene CYP707A2 and suppressed expression of the genes of GA20ox1, GA20ox2, and GA20ox5 involved in GA synthesis under salt stress, respectively. The MtCIR2-dependent enhanced endogenous ABA and reduced endogenous GA concentrations in seeds resulted in greater suppression of seed germination in transgenic seeds than in wild-type seeds when exposed to salt stress. These findings highlight a regulatory role of lncRNAs in response to salt stress during seed germination.

The regulatory role and therapeutic potential of long non-coding RNA in non-small cell lung cancer.

Lung cancer remains the leading cause of cancer-related mortality worldwide, with non-small cell lung cancer (NSCLC) being the predominant subtype. Recent advances in transcriptome sequencing have highlighted the critical role of long non-coding RNAs (lncRNAs) in NSCLC, with lncRNAs influencing gene expression through epigenetic, transcriptional, and post-transcriptional mechanisms. Despite the growing understanding of lncRNAs, challenges such as delayed diagnosis and drug resistance continue to complicate NSCLC management. This review explores novel findings in the role of lncRNAs (e.g., MALAT1, HOTAIR, and GAS5) in NSCLC, with a particular focus on their encoded small peptides and N6-methyladenosine (m6A) modifications. We further discuss how the interplay between lncRNAs, their encoded peptides, and m6A modifications can provide new strategies for improving NSCLC diagnosis, treatment, and overcoming drug resistance. This review also highlights emerging research avenues that could lead to innovative clinical interventions in NSCLC.

Spatial Expression of Long Non-Coding RNAs in Human Brains of Alzheimer's Disease.

Long non-coding RNAs (lncRNAs) are critical regulators of physiological and pathological processes, with their dysregulation increasingly implicated in aging and Alzheimer's disease (AD). Using spatial transcriptomics, we analyzed 78 postmortem brain sections from 21 ROSMAP participants to map the spatial expression of lncRNAs in the dorsolateral prefrontal cortex of aged human brains. Compared to mRNAs, lncRNAs exhibited greater subregion-specific expression, with enrichment in antisense and lincRNA biotypes. Network analysis identified 193 gene modules across eight subregions, including lncRNA-enriched modules involved in critical biological processes. We also identified AD differentially expressed (DE) lncRNAs, which showed greater subregion specificity than AD DE mRNAs. Gene set enrichment analysis highlighted the involvement of these AD DE lncRNAs in epigenetic regulation and chromatin remodeling, including enrichment for HDAC target genes such as OIP5-AS1. Statistical modeling suggested that interactions between OIP5-AS1 and HDAC proteins, particularly HDAC11, were associated with tau tangles in excitatory neurons and plaque burden in microglia. This study provides a comprehensive resource of lncRNA spatial expression in the aged human brain and uncovers potential functional roles of lncRNAs in AD pathogenesis.

Epigenetic Role of Long Non-coding RNAs in Multiple Myeloma.

This review aims to explore the pivotal role of long non-coding RNAs (lncRNAs) as epigenetic regulators in the pathogenesis of multiple myeloma (MM). Additionally, we have portrayed the dual role of lncRNAs in the epigenetic landscape of MM pathobiology. In MM, lncRNAs are pivotal for proliferation, progression, and drug resistance by acting as miRNA sponges, regulating mRNA activity through microRNA recognition elements (MREs). Epigenetic modifications in lncRNAs influence gene expression, with some like MEG3, GAS5, CRNDE, and H19 showing promoter hypermethylation, while MALAT1 exhibits hypomethylation. Targeting lncRNAs using siRNA, ASO, CRISPR-Cas9, or small molecule inhibitors shows promise in preclinical studies, alongside the potential benefits of epigenetic-based therapies such as DNMTi and HDACi. Clinical trials combining epigenetic modifiers with standard chemotherapy show encouraging results, especially in relapsed/refractory MM. The key finding of the studies highlighted in the review paves the way for understanding the epigenetic role of lncRNAs in MM disease progression and biology. In addition, the novel therapeutic strategies that have shown promising results have been highlighted. The adoption of the epigenetic landscape into therapeutics in addition to existing treatment strategies may increase the efficacy of treatment approaches.

Comprehensive transcriptome analysis reveals lncRNA-mRNA interactions and immune response mechanisms in Mytilus coruscus upon Vibrio alginolyticus infection.

Long non-coding RNAs (lncRNAs) play diverse biological roles within cells. Despite not encoding proteins, they are crucial in regulating gene expression, chromatin structure and function, cell differentiation and development, and the occurrence of diseases. Vibrio alginolyticus (V. alginolyticus) is a common bacterium found in marine environments that poses a threat to shellfish by infecting them through filtration feeding. Research has demonstrated the substantial involvement of lncRNAs in the immune response of shellfish. However, the specific mechanism by which lncRNAs participate in the immune regulatory process following infection of Mytilus coruscus (M. coruscus) with V. alginolyticus has not been investigated. Therefore, the transcription profiles of lncRNAs in M. coruscus hemocytes were investigated. A grand total of 48,246 lncRNAs were detected, with 2,421 genes that exhibited and 717 lncRNAs that had differential expression. To gain a better understanding of the potential roles of the differentially expressed lncRNAs (DE-lncRNAs), GO and KEGG pathway analyses were performed on their target mRNAs, suggesting that lncRNAs have the ability to control gene expression levels and consequently influence immune-related pathways, hence regulating the immune response in M. coruscus. Additionally, a total of 138 lncRNA-mRNA pairs were identified through the calculation of co-expression relationships between DE-lncRNAs and immune-related DE-mRNAs. These findings provide new insights into the role of lncRNAs in the immune response of M. coruscus and offer important resources for further investigation into the role of lncRNAs in M. coruscus pathogen infection.