[Retracted] LINC00665 functions as a competitive endogenous RNA to regulate AGTR1 expression by sponging miR­34a­5p in glioma.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the 'Control' data panel shown for the EdU assay experiment in Fig. 6D on p. 1209 was strikingly similar to a data panel featured in Fig. 7 that had already been submitted to the journal Cancer Management and Research by different authors at different research institutes [Chen T­J, Gao F, Yang T, Li H, Li Y, Ren H and Chen M­W: Knockdown of linc­POU3F3 suppresses the proliferation, apoptosis, and migration resistance of colorectal cancer. Cancer Manag Res 12: 4379­4390, 2020]. Owing to the fact that contentious data in the above article had already been submitted for publication prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 45: 1202­1212, 2021; DOI: 10.3892/or.2021.7949].

CircRNA and lncRNA-associated competing endogenous RNA networks in medulloblastoma: a scoping review.

BACKGROUND: Medulloblastoma is one of the common primary central nervous system (CNS) malignancies in pediatric patients. The main treatment is surgical resection preceded and/or followed by chemoradiotherapy. However, their serious side effects necessitate a better understanding of medulloblastoma biology to develop novel therapeutic options. MAIN BODY: Circular RNA (circRNA) and long non-coding RNA (lncRNA) regulate gene expression via microRNA (miRNA) pathways. Although growing evidence has highlighted the significance of circRNA and lncRNA-associated competing endogenous RNA (ceRNA) networks in cancers, no study has comprehensively investigated them in medulloblastoma. For this aim, the Web of Science, PubMed, Scopus, and Embase were systematically searched to obtain the relevant papers published before 16 September 2023, adhering to the PRISMA-ScR statement. HOTAIR, NEAT1, linc-NeD125, HHIP-AS1, CRNDE, and TP73-AS1 are the oncogenic lncRNAs, and Nkx2-2as is a tumor-suppressive lncRNA that develop lncRNA-associated ceRNA networks in medulloblastoma. CircSKA3 and circRNA_103128 are upregulated oncogenic circRNAs that develop circRNA-associated ceRNA networks in medulloblastoma. CONCLUSION: In summary, this study has provided an overview of the existing evidence on circRNA and lncRNA-associated ceRNA networks and their impact on miRNA and mRNA expression involved in various signaling pathways of medulloblastoma. Suppressing the oncogenic ceRNA networks and augmenting tumor-suppressive ceRNA networks can provide ample opportunities for medulloblastoma treatment.

The identification of biomarkers for Alzheimer's disease using a systems biology approach based on lncRNA-circRNA-miRNA-mRNA ceRNA networks.

In addition to being the most prevalent form of neurodegeneration among the elderly, AD is a devastating multifactorial disease. Currently, treatments address only its symptoms. Several clinical studies have shown that the disease begins to manifest decades before the first symptoms appear, indicating that studying early changes is crucial to improving early diagnosis and discovering novel treatments. Our study used bioinformatics and systems biology to identify biomarkers in AD that could be used for diagnosis and prognosis. The procedure was performed on data from the GEO database, and GO and KEGG enrichment analysis were performed. Then, we set up a network of interactions between proteins. Several miRNA prediction tools including miRDB, miRWalk, and TargetScan were used. The ceRNA network led to the identification of eight mRNAs, four circRNAs, seven miRNAs, and seven lncRNAs. Multiple mechanisms, including the cell cycle and DNA replication, have been linked to the promotion of AD development by the ceRNA network. By using the ceRNA network, it should be possible to extract prospective biomarkers and therapeutic targets for the treatment of AD. It is possible that the processes involved in DNA cell cycle and the replication of DNA contribute to the development of Alzheimer's disease.

ETENLNC: An end to end lncRNA identification and analysis framework to facilitate construction of known and novel lncRNA regulatory networks.

Long non-coding RNAs (lncRNAs) play crucial roles in the regulation of gene expression and maintenance of genomic integrity through various interactions with DNA, RNA, and proteins. The availability of large-scale sequence data from various high-throughput platforms has opened possibilities to identify, predict, and functionally annotate lncRNAs. As a result, there is a growing demand for an integrative computational framework capable of identifying known lncRNAs, predicting novel lncRNAs, and inferring the downstream regulatory interactions of lncRNAs at the genome-scale. We present ETENLNC (End-To-End-Novel-Long-NonCoding), a user-friendly, integrative, open-source, scalable, and modular computational framework for identifying and analyzing lncRNAs from raw RNA-Seq data. ETENLNC employs six stringent filtration steps to identify novel lncRNAs, performs differential expression analysis of mRNA and lncRNA transcripts, and predicts regulatory interactions between lncRNAs, mRNAs, miRNAs, and proteins. We benchmarked ETENLNC against six existing tools and optimized it for desktop workstations and high-performance computing environments using data from three different species. ETENLNC is freely available on GitHub: https://github.com/EvolOMICS-TU/ETENLNC.

Revealing the novel metabolism-related genes in the ossification of the ligamentum flavum based on whole transcriptomic data.

Backgrounds: The ossification of the ligamentum flavum (OLF) is one of the major causes of thoracic myelopathy. Previous studies indicated there might be a potential link between metabolic disorder and pathogenesis of OLF. The aim of this study was to determine the potential role of metabolic disorder in the pathogenesis of OLF using the strict bioinformatic workflow for metabolism-related genes and experimental validation. Methods: A series of bioinformatic approaches based on metabolism-related genes were conducted to compare the metabolism score between OLF tissues and normal ligamentum flavum (LF) tissues using the single sample gene set enrichment analysis. The OLF-related and metabolism-related differentially expressed genes (OMDEGs) were screened out, and the biological functions of OMDEGs were explored, including the Gene Ontology enrichment analysis, Kyoto Encyclopedia of Genes and Genomes enrichment analysis, and protein-protein interaction. The competing endogenous RNA (ceRNA) network based on pairs of miRNA-hub OMDEGs was constructed. The correlation analysis was conducted to explore the potential relationship between metabolic disorder and immunity abnormality in OLF. In the end, the cell experiments were performed to validate the roles of GBE1 and TNF-α in the osteogenic differentiation of LF cells. Results: There was a significant difference of metabolism score between OLF tissues and normal LF tissues. Forty-nine OMDEGs were screened out and their biological functions were determined. The ceRNA network containing three hub OMDEGs and five differentially expressed miRNAs (DEmiRNAs) was built. The correlation analysis between hub OMDEGs and OLF-related infiltrating immune cells indicated that metabolic disorder might contribute to the OLF via altering the local immune status of LF tissues. The cell experiments determined the important roles of GBE1 expression and TNF-α in the osteogenic differentiation of LF cells. Conclusions: This research, for the first time, preliminarily illustrated the vital role of metabolic disorder in the pathogenesis of OLF using strict bioinformatic algorithms and experimental validation for metabolism-related genes, which could provide new insights for investigating disease mechanism and screening effective therapeutic targets of OLF in the future.

A black phosphorus nanosheet-based RNA delivery system for prostate cancer therapy by increasing the expression level of tumor suppressor gene PTEN via CeRNA mechanism.

BACKGROUND: Prostate cancer (PCa) has a high incidence in men worldwide, and almost all PCa patients progress to the androgen-independent stage which lacks effective treatment measures. PTENP1, a long non-coding RNA, has been shown to suppress tumor growth through the rescuing of PTEN expression via a competitive endogenous RNA (ceRNA) mechanism. However, PTENP1 was limited to be applied in the treatment of PCa for the reason of rapid enzymatic degradation, poor intracellular uptake, and excessively long base sequence to be synthesized. Considering the unique advantages of artificial nanomaterials in drug loading and transport, black phosphorus (BP) nanosheet was employed as a gene-drug carrier in this study. RESULTS: The sequence of PTENP1 was adopted as a template which was randomly divided into four segments with a length of about 1000 nucleotide bases to synthesize four different RNA fragments as gene drugs, and loaded onto polyethyleneimine (PEI)-modified BP nanosheets to construct BP-PEI@RNA delivery platforms. The RNAs could be effectively delivered into PC3 cells by BP-PEI nanosheets and elevating PTEN expression by competitive binding microRNAs (miRNAs) which target PTEN mRNA, ultimately exerting anti-tumor effects. CONCLUSIONS: Therefore, this study demonstrated that BP-PEI@RNAs is a promising gene therapeutic platform for PCa treatment.

CircCUL1 inhibits trophoblast cell migration and invasion and promotes cell autophagy by sponging hsa-miR-30e-3p in fetal growth restriction via the ANXA1/PI3K/AKT axis.

Fetal growth restriction (FGR) severely affects the health outcome of newborns and represents a major cause of perinatal morbidity. The precise involvement of circCULT1 in the progression of FGR remains unclear. We performed next-generation sequencing and RT-qPCR to identify differentially expressed circRNAs in placental tissues affected by FGR by comparing them with unaffected counterparts. Edu, flow cytometry, and transwell assay were conducted to detect HTR8/SVneo cell's function in regard to cell proliferation, migration, and invasion. The interaction between circCUL1 and hsa-miR-30e-3p was assessed through dual-luciferase reporter assays, validation of the interaction between circCUL1 and ANXA1 was performed using RNA pulldown and immunoprecipitation assays. Western blot analysis was performed to evaluate protein levels of autophagy markers and components of the PI3K/AKT signaling pathway. A knockout (KO) mouse model was established for homologous mmu-circ-0001469 to assess fetal mouse growth and development indicators. Our findings revealed an upregulation of circCUL1 expression in placental tissues from patients with FGR. We found that suppression of circCUL1 increased the trophoblast cell proliferation, migration, and invasion, circCUL1 could interact with hsa-miR-30e-3p. Further, circCUL1 stimulated autophagy, modulating trophoblast cell autophagy via the ANXA1/PI3K/AKT pathway, and a notable disparity was observed, with KO mice displaying accelerated embryo development and exhibiting heavier placentas in comparison to wild-type C57BL/6 mice. By modulating the ANXA1/PI3K/AKT signaling pathway through the interaction with hsa-miR-30e-3p, circCUL1 promotes autophagy while concurrently suppressing trophoblast cell proliferation, migration, and invasion. These findings offer novel insights into potential diagnostic markers and therapeutic targets for FGR research.

Long non-coding RNA HOTTIP promotes renal cell carcinoma progression through the regulation of the miR-506 pathway.

HOXA transcript at the distal tip (HOTTIP), a lncRNA, induces cell proliferation and cancer progression. However, the expression and function of HOTTIP in renal cell carcinoma (RCC) were rarely reported. The role of the HOTTIP in RCC was explored in this study. HOTTIP expresses higher in RCC tissues than in normal tissues and indicates poor prognosis based on the TCGA database. The over- and low-expression HOTTIP cell line was established in this research to assess the oncogenic function of HOTTIP in RCC progression. Mechanistic analyses revealed that HOTTIP functioned as a competing endogenous RNA (ceRNA) for miR-506. RIP experiment and luciferase assay were performed to explore the mechanisms of the sponge between HOTTIP and miR-506. HOTTIP down-regulation attenuated cell proliferation, migration, and invasion, which could be rescued by miR-506 down-regulation. On the whole, this study revealed that the HOTTIP/miR-506 axis has a dominant impact on RCC progression and potentially provides a novel strategy for RCC diagnosis and therapy.

Identifying autophagy-related mRNAs and potential ceRNA networks in meniscus degeneration based on RNA sequencing and experimental validation.

Purpose: The intimate connection between long noncoding RNA (lncRNA) and autophagy has been established in cartilage degeneration. However, their roles in meniscal degeneration remain ambiguous. This study aimed to identify the key autophagy-related lncRNA and its associated regulatory network in meniscal degeneration in the context of osteoarthritis (OA). Methods: RNA sequencing was performed to identify differentially expressed lncRNAs (DELs) and mRNAs (DEMs), which were then conducted to enrichment analyses using the DAVID database and Metascape. Autophagy-related DEMs were identified by combining DEMs with data from the Human Autophagy Database. Three databases were used to predict miRNA, and the DIANA LncBase Predicted database was utilized to predict miRNA-lncRNA interactions. Based on these predictions, comprehensive competitive endogenous RNA (ceRNA) network were constructed. The expression levels of the classical autophagy markers and autophagy-related ceRNA network were validated. Additionally, Gene Set Enrichment Analysis (GSEA) was performed using autophagy-related DEMs. Results: 310 DELs and 320 DEMs were identified, with five upregulated and one downregulated autophagy-related DEMs. Through reverse prediction of miRNA, paired miRNA-lncRNA interactions, and verification using RT-qPCR, two lncRNAs (PCAT19, CLIP1-AS1), two miRNA (has-miR-3680-3p and has-miR-4795-3p) and two mRNAs (BAG3 and HSP90AB1) were included in the constructed ceRNA regulatory networks. GSEA indicated that the increased expression of autophagy-related mRNAs inhibited glycosaminoglycan biosynthesis in the degenerative meniscus. Conclusion: This study presented the first construction of regulatory ceRNA network involving autophagy-related lncRNA-miRNA-mRNA interactions in OA meniscus. These findings offered valuable insights into the mechanisms underlying meniscal degeneration and provided potential targets for therapeutic intervention.

Whole transcriptome analysis identifies differentially expressed mRNA, miRNA and lncRNA associated with male sterility in the silkworm, Bombyx mori.

Insect sterility technology is gradually being applied to the control of lepidoptera pests, and the target gene for male sterility is the core of this technology. JMS is a mutant silkworm that exhibits male sterility, and to elucidate its formation mechanism, this study conducted a full transcriptome analysis of the testes of JMS and its wild-type silkworms 48 h after pupation, identifying 205 DElncRNAs, 913 mRNAs, and 92 DEmiRNAs. The KEGG pathway enrichment analysis of the DEmRNAs revealed that they were involved in the biosynthesis of amino acids and ECM-receptor interactions. Combined with ceRNA regulatory network KEGG analysis suggests that pathways from amino acid biosynthesis to hydrolytic processes of protein synthesis may play a crucial role in the formation of JMS mutant variants. Our study deepens our understanding of the regulatory network of male sterility genes in silkworms; it also provides a new perspective for insect sterility technology.

Mesangial cell-derived CircRNAs in chronic glomerulonephritis: RNA sequencing and bioinformatics analysis.

BACKGROUND: Circular RNAs (circRNAs) have been shown to play critical roles in the initiation and progression of chronic glomerulonephritis (CGN), while their role from mesangial cells in contributing to the pathogenesis of CGN is rarely understood. Our study aims to explore the potential functions of mesangial cell-derived circRNAs using RNA sequencing (RNA-seq) and bioinformatics analysis. METHODS: Mouse mesangial cells (MMCs) were stimulated by lipopolysaccharide (LPS) to establish an in vitro model of CGN. Pro-inflammatory cytokines and cell cycle stages were detected by Enzyme-linked immunosorbent assay (ELISA) and Flow Cytometry experiment, respectively. Subsequently, differentially expressed circRNAs (DE-circRNAs) were identified by RNA-seq. GEO microarrays were used to identify differentially expressed mRNAs (DE-mRNAs) between CGN and healthy populations. Weighted co-expression network analysis (WGCNA) was utilized to explore clinically significant modules of CGN. CircRNA-associated CeRNA networks were constructed by bioinformatics analysis. The hub mRNAs from CeRNA network were identified using LASSO algorithms. Furthermore, utilizing protein-protein interaction (PPI), gene ontology (GO), pathway enrichment (KEGG), and GSEA analyses to explore the potential biological function of target genes from CeRNA network. In addition, we investigated the relationships between immune cells and hub mRNAs from CeRNA network using CIBERSORT. RESULTS: The expression of pro-inflammatory cytokines IL-1ß, IL-6, and TNF-α was drastically increased in LPS-induced MMCs. The number of cells decreased significantly in the G1 phase but increased significantly in the S/G2 phase. A total of 6 DE-mRNAs were determined by RNA-seq, including 4 up-regulated circRNAs and 2 down-regulated circRNAs. WGCNA analysis identified 1747 DE-mRNAs of the turquoise module from CGN people in the GEO database. Then, the CeRNA networks, including 6 circRNAs, 38 miRNAs, and 80 mRNAs, were successfully constructed. The results of GO and KEGG analyses revealed that the target mRNAs were mainly enriched in immune, infection, and inflammation-related pathways. Furthermore, three hub mRNAs (BOC, MLST8, and HMGCS2) from the CeRNA network were screened using LASSO algorithms. GSEA analysis revealed that hub mRNAs were implicated in a great deal of immune system responses and inflammatory pathways, including IL-5 production, MAPK signaling pathway, and JAK-STAT signaling pathway. Moreover, according to an evaluation of immune infiltration, hub mRNAs have statistical correlations with neutrophils, plasma cells, monocytes, and follicular helper T cells. CONCLUSIONS: Our findings provide fundamental and novel insights for further investigations into the role of mesangial cell-derived circRNAs in CGN pathogenesis.

Comprehensive analysis of miRNAs-lncRNAs-mRNAs modules and ceRNA network in acute liver failure: Hsa-miR3175 and C-reactive protein determination.

Acute liver failure (ALF), also known as fulminant hepatitis, coagulation disorders, and worsening mental status. It has a poor prognosis and high mortality rate. Among these, the top 10 upregulated genes included GKA-DPA1, IGLL5, PLA2G7, CCL5, IGLJ, GUSBP11, RHOBT1, IGLL3P, CCL18, and ADRBK2. On the other hand, the top 10 downregulated genes were SLC6A1, PID1, AVPR1A, PP1R1A, ST3GAL6, TPST, ERO1LB, SLCO4C1, and KLF15. Furthermore, the DEGs were found to be enriched in processes related to LIAO metastasis and creighton endocrine therapy resistance. To explore the interactions among the DEGs, we constructed a PPI network. This network revealed 16 hub genes that play crucial roles in ALF pathogenesis. Within this network, hsa-mir-375 and hsa-mir-650 were identified as central nodes, indicating their potential importance in ALF. By identifying and analyzing the transcriptional-level ceRNA network, we have provided valuable insights into the etiology of ALF.

Identification of necroptosis-related genes in ankylosing spondylitis by bioinformatics and experimental validation.

The pathogenesis of ankylosing spondylitis (AS) remains unclear, and while recent studies have implicated necroptosis in various autoimmune diseases, an investigation of its relationship with AS has not been reported. In this study, we utilized the Gene Expression Omnibus database to compare gene expressions between AS patients and healthy controls, identifying 18 differentially expressed necroptosis-related genes (DENRGs), with 8 upregulated and 10 downregulated. Through the application of three machine learning algorithms-least absolute shrinkage and selection operation, support vector machine-recursive feature elimination and random forest-two hub genes, FASLG and TARDBP, were pinpointed. These genes demonstrated high specificity and sensitivity for AS diagnosis, as evidenced by receiver operating characteristic curve analysis. These findings were further supported by external datasets and cellular experiments, which confirmed the downregulation of FASLG and upregulation of TARDBP in AS patients. Immune cell infiltration analysis suggested that CD4+ T cells, CD8+ T cells, NK cells and neutrophils may be associated with the development of AS. Notably, in the group with high FASLG expression, there was a significant infiltration of CD8+ T cells, memory-activated CD4+ T cells and resting NK cells, with relatively less infiltration of memory-resting CD4+ T cells and neutrophils. Conversely, in the group with high TARDBP expression, there was enhanced infiltration of naïve CD4+ T cells and M0 macrophages, with a reduced presence of memory-resting CD4+ T cells. In summary, FASLG and TARDBP may contribute to AS pathogenesis by regulating the immune microenvironment and immune-related signalling pathways. These findings offer new insights into the molecular mechanisms of AS and suggest potential new targets for therapeutic strategies.

Effect of ZIC2 on immune infiltration and ceRNA axis regulation in lung adenocarcinoma via bioinformatics and experimental studies.

OBJECTIVE: This study aimed to conclude the effect and mechanism of ZIC2 on immune infiltration in lung adenocarcinoma (LUAD). METHODS: Expression of ZIC2 in several kinds of normal tissues of TCGA data was analyzed and its correlation with the baseline characteristic of LUAD patients were analyzed. The immune infiltration analysis of LUAD patients was performed by CIBERSORT algorithm. The correlation analysis between ZIC2 and immune cell composition was performed. Additionally, the potential upstream regulatory mechanisms of ZIC2 were predicted to identify the possible miRNAs and lncRNAs that regulated ZIC2 in LUAD. In vitro and in vivo experiments were also conducted to confirm the potential effect of ZIC2 on cell proliferation and invasion ability of LUAD cells. RESULTS: ZIC2 expression was decreased in various normal tissues, but increased in multiple tumors, including LUAD, and correlated with the prognosis of LUAD patients. Enrichment by GO and KEGG suggested the possible association of ZIC2 with cell cycle and p53 signal pathway. ZIC2 expression was significantly correlated with T cells CD4 memory resting, Macrophages M1, and plasma cells, indicating that dysregulated ZIC2 expression in LUAD may directly influence immune infiltration. ZIC2 might be regulated by several different lncRNA-mediated ceRNA mechanisms. In vitro experiments validated the promotive effect of ZIC2 on cell viability and invasion ability of LUAD cells. In vivo experiments validated ZIC2 can accelerate tumor growth in nude mouse. CONCLUSION: ZIC2 regulated by different lncRNA-mediated ceRNA mechanisms may play a critical regulatory role in LUAD through mediating the composition of immune cells in tumor microenvironment.

Identification of ceRNA networks in type H and L vascular endothelial cells through integrated bioinformatics methods. / 通过整合的生物信息学方法鉴定H和Låž‹è¡€ç®¡å† çš®ç»†èƒžä¸­çš„ceRNA网络（英文）.

OBJECTIVES: Type H blood vessels are a subtype of bone-specific microvessels (CD31hiEmcnhi) that play an important regulatory role in the coupling of angiogenesis and osteogenesis. Despite reports on the distinct roles of type H and L vessels under physiological and pathological bone conditions, their genetic differences remain to be elucidated. This study aims to construct a competitive endogenous RNA (ceRNA) network of key gene for differencial expression (DE) in type H and L vascular endothelial cells (ECs) through integrated bioinformatic methods. METHODS: We downloaded relevant raw data from the ArrayExpress and the Gene Expression Omnibus (GEO) database and used the Limma R-Bioconductor package to screen for DE lncRNAs, DE miRNAs, and DE mRNAs between type H and L vascular ECs. A total ceRNA network was constructed based on their interactions, followed by refinement using protein-protein interaction (PPI) networks to select upregulated and downregulated key genes. Enrichment analysis was performed on these key genes. Random validation was conducted using flow cytometry and real-time RT-PCR. RESULTS: A total of 1 761 DE mRNAs, 187 DE lncRNAs, and 159 DE miRNAs were identified, and a comprehensive ceRNA network was constructed based on their interactions. Six upregulated (Itga5, Kdr, Tjp1, Pecam1, Cdh5, and Ptk2) and 2 downregulated (Csf1r and Il10) key genes were selected via PPI network to construct a subnetwork of ceRNAs related to these key genes. Upregulated key genes were mainly enriched in negative regulation of angiogenesis and vascular apoptosis. Results from flow cytometry and real-time RT-PCR were consistent with bioinformatics analysis. CONCLUSIONS: This study proposes a ceRNA network associated with upregulated and downregulated type H and L vascular ECs based on selected key genes, providing new insights into the regulatory mechanisms of type H and L vascular ECs in bone metabolism.

Comprehensive analysis of ceRNA network and immune cell infiltration pattern of autophagy related genes in IgA nephropathy.

INTRODUCTION: IgA nephropathy (IgAN) is a prevalent worldwide glomerular disease with a complex pathophysiology that has significant economic implications. Despite the lack of successful research, this study aims to discover the potential competing endogenous RNA (ceRNA) network of autophagy-associated genes in IgAN and examine their correlation with immune cell infiltration. METHODS: Autophagy-related hub genes were discovered by assessing the GSE116626 dataset and constructing a protein-protein interaction network. Nephroseq v5 analysis engine was used to analyze correlations between hub genes and proteinuria, glomerular filtration rate (GFR) and serum creatinine levels. Then, a ceRNA network construction and the CIBERSORT tool for immune cell infiltration analysis were also performed. Additionally, the differentially expressed autophagy-related genes (DEARGs) were used to predict potential targeted medications for IgAN. RESULTS: 1396 differentially expressed genes (DEGs) were identified in IgAN along with 25 autophagy-related differentially expressed messenger RNAs (DEmRNAs). Enrichment analysis revealed significant involvement of autophagy and apoptosis in biological processes. Next, we evaluated the top hub nodes based on their highest degrees. The ability of IgAN discrimination was confirmed in the GSE35487 and GSE37460 datasets by validating the five hub genes: SIRT1, FOS, CCL2, CDKN1A and MYC. In the Nephroseq v5 analysis engine, the clinical correlation of the five hub genes was confirmed. Furthermore, the ceRNA network identified 18 circular RNAs and 2 microRNAs associated with hub autophagy-related genes in IgAN. Our investigation identified hsa-miR-32-3p and hsa-let-7i-5p as having elevated expression levels and substantial diagnostic value. Finally, four distinctively infiltrated immune cells were found to be associated with the hub autophagy-related genes, and 67 drugs were identified as potential therapeutic options for IgAN. CONCLUSION: This study sheds light on a novel ceRNA regulatory network mechanism associated with autophagy in IgAN development.

Comprehensive analysis of the expression profiles of mRNA, lncRNA, circRNA, and miRNA in primary hair follicles of coarse sheep fetal skin.

BACKGROUND: The Qinghai Tibetan sheep, a local breed renowned for its long hair, has experienced significant deterioration in wool characteristics due to the absence of systematic breeding practices. Therefore, it is imperative to investigate the molecular mechanisms underlying follicle development in order to genetically enhance wool-related traits and safeguard the sustainable utilization of valuable germplasm resources. However, our understanding of the regulatory roles played by coding and non-coding RNAs in hair follicle development remains largely elusive. RESULTS: A total of 20,874 mRNAs, 25,831 circRNAs, 4087 lncRNAs, and 794 miRNAs were annotated. Among them, we identified 58 DE lncRNAs, 325 DE circRNAs, 924 DE mRNAs, and 228 DE miRNAs during the development of medullary primary hair follicle development. GO and KEGG functional enrichment analyses revealed that the JAK-STAT, TGF-ß, Hedgehog, PPAR, cGMP-PKG signaling pathway play crucial roles in regulating fibroblast and epithelial development during skin and hair follicle induction. Furthermore, the interactive network analysis additionally identified several crucial mRNA, circRNA, and lncRNA molecules associated with the process of primary hair follicle development. Ultimately, by investigating DEmir's role in the ceRNA regulatory network mechanism, we identified 113 circRNA-miRNA pairs and 14 miRNA-mRNA pairs, including IGF2BP1-miR-23-x-novel-circ-01998-MSTRG.7111.3, DPT-miR-370-y-novel-circ-005802-MSTRG.14857.1 and TSPEAR-oar-miR-370-3p-novel-circ-005802- MSTRG.10527.1. CONCLUSIONS: Our study offers novel insights into the distinct expression patterns of various transcription types during hair follicle morphogenesis, establishing a solid foundation for unraveling the molecular mechanisms that drive hair development and providing a scientific basis for selectively breeding desirable wool-related traits in this specific breed.

CircWHSC1 (CircNSD2): A Novel Circular RNA in Multiple Cancers.

Circular RNAs (circRNAs) are a type of non-coding RNA (ncRNA) that possesses a unique single-stranded circular structure. They are primarily formed through alternative splicing of pre-mRNA (messenger RNA). The primary biological function of circRNAs is to regulate gene expression at both the transcriptional and post-transcriptional levels. Recent studies have increasingly demonstrated a close association between the dysregulation of circRNAs and the progression of diverse cancers, where they can function as either tumor suppressors or oncogenes. circWHSC1 (circNSD2) is a circular ncRNA that originates from the first 2 exons of the Wolf-Hirschhorn syndrome candidate gene (WHSC1). As Chen 2019 discovery that circWHSC1 (circNSD2) functions as a sponge for miRNAs and promotes cancer, this circRNA has garnered significant interest among researchers. circWHSC1 (circNSD2) has been found to be up-regulated in various malignant tumors, including nasopharyngeal carcinoma, lung cancer, breast cancer, liver cancer, colorectal cancer, ovarian cancer, cervical cancer, and endometrial cancer. It exerts its effects on cancer by either inhibiting or promoting the expression of related genes through direct or indirect pathways, ultimately affecting cancer proliferation, invasion, and prognosis. This article provides a comprehensive review and discussion of the biological roles of circWHSC1 (circNSD2) and its target genes in various cancers, as well as the latest research progress on related molecular biological regulatory mechanisms. Furthermore, the potential significance of circWHSC1 (circNSD2) in future clinical applications and transformations is thoroughly analyzed and discussed.

Tweety homolog 3 promotes colorectal cancer progression through mutual regulation of histone deacetylase 7.

Colorectal cancer (CRC) is one of the leading cancers worldwide, with metastasis being a major cause of high mortality rates among patients. In this study, dysregulated gene Tweety homolog 3 (TTYH3) was identified by Gene Expression Omnibus database. Public databases were used to predict potential competing endogenous RNAs (ceRNAs) for TTYH3. Quantitative real-time polymerase chain reaction, western blot, and immunohistochemistry were utilized to analyze TTYH3 and histone deacetylase 7 (HDAC7) levels. Luciferase assays confirmed miR-1271-5p directly targeting the 3' untranslated regions of TTYH3 and HDAC7. In vitro experiments such as transwell and human umbilical vein endothelial cell tube formation, as well as in vivo mouse models, were conducted to assess the biological functions of TTYH3 and HDAC7. We discovered that upregulation of TTYH3 in CRC promotes cell migration by affecting the Epithelial-mesenchymal transition pathway, which was independent of its ion channel activity. Mechanistically, TTYH3 and HDAC7 functioned as ceRNAs, reciprocally regulating each other's expression. TTYH3 competes for binding miR-1271-5p, increasing HDAC7 expression, facilitating CRC metastasis and angiogenesis. This study reveals the critical role of TTYH3 in promoting CRC metastasis through ceRNA crosstalk, offering new insights into potential therapeutic targets for clinical intervention.

Integrative ceRNA network analysis identifies unique and shared molecular signatures in Bipolar Disorder and Schizophrenia.

Bipolar Disorder (BPD) and Schizophrenia (SCZ) are complex psychiatric disorders with shared symptomatology and genetic risk factors. Understanding the molecular mechanisms underlying these disorders is crucial for refining diagnostic criteria and guiding targeted treatments. In this study, publicly available RNA-seq data from post-mortem samples of the basal ganglia's striatum were analyzed using an integrative computational approach to identify differentially expressed (DE) transcripts associated with SCZ and BPD. The analysis aimed to reveal both shared and distinct genes and long non-coding RNAs (lncRNAs) and to construct competitive endogenous RNA (ceRNA) networks within the striatum. Furthermore, the functional implications of these identified transcripts are explored, alongside their presence in established databases such as BipEx and SCHEMA. A significant outcome of our analysis was the identification of 21 DEmRNAs and 1 DElncRNA shared between BPD and SCZ across the Caudate, Putamen, and Nucleus Accumbens. Another noteworthy finding was the identification of Hub nodes within the ceRNA networks that were linked to major psychosis. Particularly, MED19, HNRNPC, MAGED4B, KDM5A, GOLGA7, CHASERR, hsa-miR-4778-3p, hsa-miR-4739, and hsa-miR-4685-5p emerged as potential biomarkers. These findings shed light on the common and unique molecular signatures underlying BPD and SCZ, offering significant potential for the advancement of diagnostic and therapeutic strategies tailored to these psychiatric disorders.