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Results for “long intergenic noncoding RNAs”

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7 recordsLinked to original sources
PubMed2026

Overexpression of a subset of long intergenic noncoding RNAs in uterine serous carcinoma predicts poor prognosis.

The evaluation and prediction of uterine serous carcinoma (USC), a type of endometrial cancer that is more severe than endometrioid adenocarcinoma, remain challenging. Long noncoding RNAs (lncRNAs) are frequently dysregulated in human cancers. This study assessed the expression patterns and prognostic values of long intergenic noncoding RNAs (lincRNAs) in USC. RNA sequencing, copy number variation (CNV), and clinical data from The Cancer Genome Atlas were used to investigate various lncRNAs in endometrial cancer. LincRNAs, a major subclass of lncRNAs, exhibit specific expression patterns modulated by CNVs and act as predictors of poor prognosis, survival, and recurrence in USC. Functional analyses were conducted to investigate the roles of lncRNAs in USC. Finally, the expression of these lincRNAs was verified in 32 pairs of USCs collected from the hospital over 3 years. A series of lincRNAs were found to be specifically expressed in USC compared with other lncRNAs and regulated by CNV. Moreover, these specific upregulated lincRNAs, particularly ENSG00000281406, ENSG00000226791, ENSG00000269903, and ENSG00000204277, demonstrated poor prognoses for survival and recurrence in USC. Functionally, our analysis showed that ENSG00000281406 positively correlated with the Wnt signaling pathway, whereas ENSG00000226791, ENSG00000269903, and ENSG00000204277 negatively correlated with the T-cell receptor signaling pathway. Importantly, we confirmed that ENSG00000204277 negatively correlated with CD8+ T-cell immune infiltration in USC. Our results highlight that these lincRNAs can serve as new biomarkers for the prognostic prediction of USC. In particular, ENSG00000204277 may be used as a therapeutic target for USC.

Humans↗
PubMed2024

Long noncoding RNA LIRIL2R modulates FOXP3 levels and suppressive function of human CD4+ regulatory T cells by regulating IL2RA.

Regulatory T cells (Tregs) are central in controlling immune responses, and dysregulation of their function can lead to autoimmune disorders or cancer. Despite extensive studies on Tregs, the basis of epigenetic regulation of human Treg development and function is incompletely understood. Long intergenic noncoding RNAs (lincRNA)s are important for shaping and maintaining the epigenetic landscape in different cell types. In this study, we identified a gene on the chromosome 6p25.3 locus, encoding a lincRNA, that was up-regulated during early differentiation of human Tregs. The lincRNA regulated the expression of interleukin-2 receptor alpha (IL2RA), and we named it the lincRNA regulator of IL2RA (LIRIL2R). Through transcriptomics, epigenomics, and proteomics analysis of LIRIL2R-deficient Tregs, coupled with global profiling of LIRIL2R binding sites using chromatin isolation by RNA purification, followed by sequencing, we identified IL2RA as a target of LIRIL2R. This nuclear lincRNA binds upstream of the IL2RA locus and regulates its epigenetic landscape and transcription. CRISPR-mediated deletion of the LIRIL2R-bound region at the IL2RA locus resulted in reduced IL2RA expression. Notably, LIRIL2R deficiency led to reduced expression of Treg-signature genes (e.g., FOXP3, CTLA4, and PDCD1), upregulation of genes associated with effector T cells (e.g., SATB1 and GATA3), and loss of Treg-mediated suppression.

Humans↗
PubMed2026

THE1 repeats: Ancient endogenous retroviruses rampaging behind sarcoid myopathy.

Transposon-like human element (THE1) repeats are classified as part of the ERVL (endogenous retrovirus-like) -MaLR family and were previously thought to be remnants derived from retroviral infections in the germ cells of ancient primates. At present, at least 60,561 THE1 repeats have been mapped in the human genome, and they are divided into four subfamilies: THE1A, THE1B, THE1C, and THE1D. Although these repeats are largely silenced in somatic cells through multiple mechanisms, some of them are known to influence gene functions and genomic structures, particularly under disease conditions. Recently, we happened to identify the CIR1 driven from THE1B in the individuals with sarcoid myopathy (SM), which is characterized by the non-caseating granulomatous inflammation recognized in skeletal muscles biopsy. Retrotrans-genomics based on the COFFEE method showed that various THE1B fusion transcripts (THE1B/FTs) and retrotransposon-associated genomic dynamics in muscle of SM, including (1) splicing of THE1B to neighborhood exons, (2) expression of THE1B associated long noncoding RNAs in the intergenic regions, (3) ectopic expression of tissue specific transcripts driven by THE1B in SM, and (4) identification of a read through transcript, SIRPB1-SIRPD. Seven of eight THE1B/FTs downregulated by tofacitinib in cutaneous sarcoidosis were confined to the granuloma associated macrophage in sarcoidosis. The remaining transcript, SMFT4 exhibited stronger expression in mesenchymal stem cells. In addition, ectopic co-expression of canonical and LINE1 and THE1A-exonizing IL23R transcripts were identified in SM. This directory of THE1B/FTs in SM may serve as a fundamental molecular basis for understanding the pathogenesis of sarcoidosis.

Journal Article↗
PubMed2026

Contrasting regulation of protein-coding genes and lncRNA homeologs in allotetraploid Coffea arabica.

A chromosome-level Bourbon assembly revealed that protein-coding homeologs are predominantly co-regulated between subgenomes. In contrast, intergenic lncRNAs display a modest, but statistically consistent bias toward subgenome E across diverse developmental and stress contexts. Coffea arabica is an allotetraploid species derived from natural hybridization between C. canephora and C. eugenioides, which contributed the C and E subgenomes, respectively. This genomic origin poses major challenges for genome assembly, annotation, and the interpretation of gene regulation. In this study, a high-quality genome assembly of C. arabica was generated and annotated, with particular emphasis on identifying protein-coding genes and intergenic long non-coding RNAs (lincRNAs). Homeologous relationships between genes from the C and E subgenomes were established, providing a robust framework to investigate subgenomic conservation and regulatory divergence. Using an extensive collection of publicly available RNA-seq libraries spanning multiple developmental stages, tissues, and environmental conditions, the relative transcriptional contribution of each subgenome was evaluated. On a global scale, gene expression was largely balanced between subgenomes, with no consistent evidence of subgenome dominance. While protein-coding genes showed comparable regulatory behavior across subgenomes, lincRNAs exhibited a more asymmetric expression pattern, suggesting higher subgenome-specific expression that is interpreted here as a consistent directional tendency rather than as evidence of subgenome dominance. Together, these results provide new insights into the regulatory architecture of the C. arabica genome and establish a foundational genomic and transcriptomic resource for future functional studies and crop improvement efforts.

Coffea↗
PubMed2026

Exploring the Effect of Whole-Genome Duplication on Salmonid LincRNA Repertoire.

Long intergenic non-coding RNAs (lincRNAs) are key epigenetic regulators of genome function, yet their evolutionary dynamics following whole-genome duplication (WGD) events remain poorly understood. Salmonids, which underwent a lineage-specific autotetraploidization (salmonid-specific WGD, ~88-100 million years ago), provide an excellent model to investigate the retention, divergence, and functional potential of recently duplicated non-coding elements. LincRNA repertoires were compared across five genome-annotated salmonids (Oncorhynchus tshawytscha, O. kisutch, O. mykiss, Salmo salar, and S. trutta) and their closest non-duplicated relative, northern pike (Esox lucius). LincRNAs represented ~5-7% of annotated genes in all salmonids except S. salar (18%). Sequence conservation was low relative to coding genes, with only 11-68 highly similar (e-value < 1 &#xd7; 10-30; similarity > 70% and alignments > 100 nucleotides) putative orthologues shared between salmonids and northern pike, and 161-338 among salmonids alone. Synteny conservation was modest in lincRNAs, with lower conservation in putative orthologues (8-16%) compared to putative ohnologues (8-33%). Secondary structure conservation was associated with sequence similarity (&#x3c1; = -0.45; p = 2.2 &#xd7; 10-16), and the association was stronger among WGD ohnologues than orthologues. In S. salar and O. mykiss, lincRNA putative ohnologues showed weaker expression correlations than coding genes, suggesting widespread regulatory divergence, possibly through neo- and subfunctionalisation. Conserved salmonid lincRNAs showed enriched predicted interactions with miRNAs involved in tumour suppression, brain, bone, and muscle development (e.g., miR-455, miR-365, miR124, miR-133a, miR-140, and miR-9), a finding supported by limited transcriptomic data. Although salmonid WGD expanded lincRNA repertoires, lincRNAs have undergone rapid sequence and transcriptional divergence, with limited conservation across species based on sequence similarity, chromosomal position, synteny, and secondary structure. A subset of conserved lincRNAs retains structural features and regulatory signatures consistent with roles as miRNA sponges in brain, skeletal, and muscle development and tumour suppression, potentially acting within conserved regulatory networks. These findings provide new insights into lincRNA evolution following genome duplication and highlight the need for experimental validation of their regulatory functions.

Animals↗
PubMed2024

Exploring the transcriptional cooperation between RUNX2 and its associated elncRNA RAIN.

Recent insights into the mechanisms controlling gene expression identified enhancer-associated long non-coding RNAs (elncRNAs) as master players of transcription in cancers. RUNX2, a mammalian RUNT-related transcription factor, is increasingly recognized in cancer biology for its role in supporting survival and progression also in thyroid cancer (TC). We recently identified, within the RUNX2 locus, a novel elncRNA that we named RAIN (RUNX2 associated intergenic lncRNA). We showed that RAIN and RUNX2 expression correlate in TC, both in vitro and in vivo, and that RAIN promotes RUNX2 expression by interacting with and affecting the activity of the RUNX2 P2 promoter through two distinct mechanisms. Here, we took forward these observations to explore the genome-wide transcriptional function of RAIN and its contribution to the RUNX2-dependent gene expression program in TC. By combining multiple omics data, we demonstrated that RAIN functionally cooperates with RUNX2 to the regulation of a subset of functionally related genes involved in promoting matrix remodeling, migration, and loss of differentiation. We showed that RAIN interacts with RUNX2 and its expression is required for the efficient recruitment of this TF to its target regulatory regions. In addition, our data revealed that besides RUNX2, RAIN governs a hierarchically organized complex transcriptional program by controlling a core of cancer-associated TFs that, in turn, orchestrate the expression of downstream genes. This evidence indicates that the functional cooperation observed between RAIN and RUNX2 can be a diffuse work mechanism for this elncRNA.

Core Binding Factor Alpha 1 Subunit↗
PubMed2020

LINC00922 regulates epithelial-mesenchymal transition, invasive and migratory capacities in breast cancer through promoting NKD2 methylation.

Breast cancer ranks as the major reason for mortality in women populations, accounting for 23% of all cancer deaths. One in every three Asian women encounters the risk of this cancer in their lifetime. Long intergenic non-coding RNAs (lincRNAs) have emerged as tumor promoters and suppressors. The molecular mechanism of breast cancer remains elusive. Therefore, the current study aimed to explore the role lincRNA LINC00922 plays in the development of breast cancer. Breast cancer tissues and adjacent tissues were obtained from 109 patients with breast cancer. The RNA extraction and quantification and immunohistochemical staining characterized the high expression of LINC00922 and low expression of NKD2 in breast cancer tissues in comparison to its adjacent counterparts. Furthermore, the ectopic expression and knockdown experiments were conducted to figure out the in vivo and in vitro effects of LINC00922 on breast cancer progression. The ectopically expressed LINC00922 activated the Wnt signaling pathway, promoted epithelial-mesenchymal transition, cell proliferative, invasive and migratory capacities, tumor growth and metastasis. Additionally, the RIP and ChIP assay identified that LINC00922 recruited DNMT1, DNMT3A and DNMT3B proteins in the promoter region of NKD2 to promote NKD2 promoter methylation, thus reducing the NKD2 expression. Moreover, the Wnt signaling pathway was activated subsequent to NKD2 silencing, which was reversed by LINC00922 silencing. Lastly, the anti-oncogenic effects of LINC00922 inhibition was antagonized after NKD2 knocked down. The current study provides evidence that LINC00922 acts as a tumor promoter by promoting NKD2 methylation. Hopefully, it provides a novel potential gene target for the treatment of breast cancer.

Adaptor Proteins, Signal Transducing↗