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Hypertrophic cardiomyopathies (HCMs) are among the most common genetic disorders; however, they might be underdiagnosed. Sequencing core sarcomere gene panels remain the main diagnostic tool. We present the results of HCM genetic testing performed at Lithuania's tertiary care center. All patients with diagnosed or clinically suspected HCM underwent next-generation panel sequencing. Of 204 patients, 34 (16.7%) received a genetic diagnosis. The most commonly affected genes were Show less

Endometriosis has a significant impact on the social, psychological, psychosomatic, and physical aspects of women's lives. There is increasing evidence that endometriosis has to be seen as a systemic and complex disorder with a multifactorial etiology, accompanied by numerous other pathologies, such as mental disorders and even cancer. Herein, we analyzed Disability-Adjusted Life Years (DALYs) and Years Lived with Disability (YLDs) generated from the Global Burden of Disease Study (GBD 2021), which are key metrics used to measure the worldwide impact of diseases. Besides, differential gene expression data generated from the Turku Endomet Database were calculated. Briefly, log2-transformed gene expression counts were investigated using linear modeling with the function expression ~ condition to generate log2 fold changes and Show less

Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is an RNA-binding protein known to play critical roles in metabolism, cell proliferation, and tumorigenesis. Although its involvement in muscle development has been documented in several species, the function of goose IGF2BP2 remains largely unexplored. In this study, we cloned and characterized the full-length cDNA and genomic DNA sequences of goose IGF2BP2. The cDNA is 2957 bp in length and contains a 1662 bp open reading frame encoding a 553-amino acid protein with five conserved RNA-binding domains. The genomic sequence spans 12,183 bp and consists of 12 exons and 11 introns. A total of 60 genetic variants were identified, including a deletion of a G base at position 2299 (g.2299delG) that results in a frameshift mutation. Expression analysis revealed high levels of IGF2BP2 mRNA in the liver, heart, and muscle tissues of female geese across embryonic (E25d), growing (A70d), and laying (L270d) stages, consistent with a potential role in muscle development ( Show less

An acute increase of lipids in the upper small intestine (USI) of rodents and humans triggers lipid-sensing pathways to reduce food intake. However, USI lipid sensing does not reduce feeding in high-fat (HF) fed conditions, and the underlying mechanism remains elusive. Here, we report that HF feeding in male rats impaired USI lipid infusion to stimulate glucose-dependent insulinotropic polypeptide (GIP) secretion and decrease refeeding, and the defects of USI lipid sensing were restored by metformin. Next, we found that infusion of GIP receptor (GIPR) agonist in the nucleus of the solitary tract (NTS), but not mediobasal hypothalamus or area postrema, resulted in decreased refeeding in chow-fed rats. The anorectic effect of NTS GIPR agonist remained intact in HF rats and was inhibited by a genetic knockdown of GIPR. Finally, an inhibition of NTS GIPR also negated the ability of USI lipid sensing with metformin to decrease refeeding despite an increase in plasma GIP levels in HF rats. Thus, USI lipid sensing in HF rats is enhanced by metformin to trigger an endocrine GIP to NTS GIPR axis to reduce food intake, thereby unveiling small intestinal lipid-sensing pathways as potential targets to enhance GIP action and reduce weight in obesity. High-fat (HF) feeding in rats impairs upper small intestine (USI) lipid sensing to increase plasma glucose-dependent insulinotropic polypeptide (GIP) levels and reduce feeding. Metformin enhances USI lipids to increase GIP and reduce feeding in HF-fed rats. GIP activates the GIP receptor (GIPR) in the nucleus of the solitary tract (NTS), which reduces food intake in HF-fed rats. GIPR in the NTS is required for small intestinal lipids with metformin to reduce feeding. Show less

In quest of new and potent multitarget therapeutics for Alzheimer's disease (AD), a series of recently synthesized arylidene-hydrazinyl-thiazoles were repurposed as multitarget directed anti-AD agents. In total, 14 compounds were tested for their inhibitory activities against the key enzymes acetylcholinesterase (AChE), β-secretase 1 (BACE1), and butyrylcholinesterase (BChE). Derivatives Show less

Recent studies have shown glycerolipid metabolism played an essential role in multiple tumors, however, its function in osteosarcoma is unclear. This study aimed to explore the role of glycerolipid metabolism in osteosarcoma. We conducted bioinformatics analysis using data from the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) database and single-cell RNA sequencing. Least Absolute Shrinkage and Selection Operator (LASSO) regression was used to identify the Glycerolipid metabolism-related genes associated with the clinical outcome of osteosarcoma. Tumor-associated macrophages (TAMs) and their interactions with immune cells were examined through single-cell analysis and co-culture experiments. Virtual screening was employed to identify the potential lysophosphatidic acid receptor 6 (LPAR6) inhibitors. Glycerolipid metabolism-related genes 1-acylglycerol-3-phosphate O-acyltransferase 3 ( Show less

Small ruminant lentivirus (SRLV) infections occur worldwide in goats and sheep and have negative impact on the production and welfare of animals. During recent years, many studies have focused on the host factors that determine the resistance of individual animals to SRLV infection; consideration of such factors would be an alternative to current control programmes based on culling seropositive animals. The aim of this study was to analyse the relationship between the expression of two previously selected goat genes, Primary fibroblast cultures obtained from the skin of goats with high SRLV proviral DNA load (HPL), low proviral load (LPL) or free of infection were inoculated with the A5 SRLV subtype circulating in the flock. The course of infection was observed based on cytopathic changes in cell cultures and the presence of SRLV A5 RNA, of which the level was monitored using a quantitative reverse-transcription PCR. The relative expression of the selected host genes following SRLV infection was analysed. The kinetics of SRLV replication differed, and distinctly higher numbers of SRLV particles were detected in cells derived from the HPL animal. The expression profiles of The observed relationship between expression of Show less

Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein particle composed of apolipoprotein B-100 covalently linked to apolipoprotein(a) [apo(a)] via a disulfide bond. The Lp(a) particle is enriched with oxidized phospholipids (OxPLs), which confer enhanced atherogenic and pro-inflammatory properties compared with low-density lipoprotein (LDL). Robust genetic and epidemiologic evidence demonstrates that elevated Lp(a) levels are independently associated with atherosclerotic cardiovascular disease and calcific aortic valve stenosis. However, no pharmacologic therapy has yet been approved that specifically lower Lp(a) or to demonstrate a reduction in cardiovascular events. Antisense oligonucleotides (e.g., pelacarsen), small-interfering RNAs (e.g., olpasiran, lepodisiran, and zerlasiran), and oral small-molecule Lp(a) inhibitors (e.g., muvalaplin) have demonstrated profound reductions in circulating Lp(a) concentrations, typically achieving decreases of 80-90%. In some studies, the reductions approached or achieved a near-complete suppression. Current genetic and modeling evidence suggests that an absolute reduction of at least 50 mg/dL in Lp(a) levels is required to achieve meaningful cardiovascular benefits. Large-scale outcome trials are now underway to assess the effects of these emerging therapies on cardiovascular and valvular outcomes. Early findings indicate favorable effects on oxidized phospholipids and vascular inflammation, suggesting broader anti-atherogenic potential. As these agents progress toward clinical use, routine Lp(a) measurement and risk stratification will become increasingly essential for personalized cardiovascular prevention. This review summarizes the molecular biology of Lp(a), highlights the limitations of current therapies, and discusses emerging RNA-based and small-molecule approaches with the potential to redefine the management of residual cardiovascular risk. Show less

The detection of circulating tumor cells (CTCs) using immunoaffinity-based methods often relies on epithelial-related markers, which may bias the selection of CTCs and limit the biological information obtained, depending on the targeted antigens. Herein, we compared the molecular profiles and clinical significance of CTCs based on the expression of epithelial-related markers ( Show less

Parkinson's disease (PD) is a complex neurodegenerative disease that involves many interlinking pathways and genetic elements that remain to be fully understood and characterised. Non-coding genetic elements have long been overlooked, however recent advancements in the field have highlighted their importance with an area of interest being transposable elements. SINE-VNTR-Alu (SVA) elements are the youngest and smallest subset of retrotransposons that are only found within hominid species. SVAs have been shown to have strong regulatory impacts within our genome and can affect progression of neurodegenerative disease such as PD. Previous studies identified an SVA, polymorphic for its presence/absence, that was associated with changes in gene expression at the Show less

Alzheimer's disease (AD) is a neurodegenerative disorder marked by a decline in cognitive function and memory loss, primarily resulting from cholinergic dysfunction, the accumulation of amyloid plaques, the formation of tau tangles, and the progressive degeneration of neurons. While existing treatments offer limited symptomatic relief, they do not effectively halt or reverse the underlying progression of the disease, presenting a major global challenge in Alzheimer's research. Developing therapeutic strategies for AD remains complex, largely due to the inability of current medications to significantly slow neurodegeneration. Traditional drug discovery processes are often lengthy, costly, and inefficient, further complicating the search for effective treatments. To overcome these obstacles, researchers have turned to a combination of computational approaches alongside conventional drug design techniques. These integrated methodologies help accelerate the discovery process by significantly reducing both time and costs. This review delves into the underlying physiological and pathological mechanisms of Alzheimer's disease, while identifying potential drug targets such as acetylcholinesterase, butyrylcholinesterase, β-Secretase (BACE-1), A2A adenosine receptor, Dickkopf-1 protein, glycogen synthase kinase-3β, indoleamine 2,3-dioxygenase, monoamine oxidase-B, NMDA receptor, Wnt inhibitory factor, cyclindependent kinase-5, glutaminyl cyclase, and cathepsin-B. Furthermore, the review examines various computer-aided drug design (CADD) methodologies, including structure-based and ligandbased approaches, virtual screening, pharmacophore modeling, molecular modelling, and simulation techniques. These computational strategies are playing an increasingly important role in Alzheimer's research, particularly in drug discovery. By investigating promising drug candidates and lead molecules that target key proteins involved in Alzheimer's pathogenesis, the review highlights their binding modes with these targets and assesses the chemical properties essential for the development of effective clinical candidates. The aim is to provide researchers with critical insights and tools to design novel compounds with the necessary chemical and physical characteristics required for the successful treatment of Alzheimer's disease. Show less

The paper is aimed to screen the target molecules of miR-12 and to further explore the mechanism of GAS5 action in prostate cancer. The expression of GPRC5B in prostate cancer cell lines LNCaP, VCaP, 22RV1, DU145, and PC3 was measured by quantitative real-time PCR with reverse transcription (RT-qPCR) and variations in GPRC5B expression were analyzed after down-regulating GAS5 or silencing miR-12. CCK8 and plate clone experiments were performed to detect changes in proliferative activity and colony-forming capacity of prostate cancer cells after down-regulating GPRC5B. After transfection of prostate cancer cells with sh-GAS5 and/or miR-12 inhibitor, the changes in GPRC5B expression were evaluated with RT-qPCR and Western blotting. Our results showed that GPRC5B was highly expressed in prostate cancer cell lines. Down-regulating of GAS5 decreased GPRC5B expression, while silencing miR-12 increased it. CCK8 and plate clone experiments showed that expression of GPRC5B increased proliferative activity and clone formation ability of prostate cancer cells. RT-qPCR and Western blotting revealed that miR-12 inhibited the promoting effect of GAS5 on GPRC5B expression. Thus, GPRC5B is directly bound to miR-12. GAS5 promotes proliferation, migration, and invasion of prostate cancer cells and participates in malignant progression of tumors by suppressing miR-12-mediated regulation of GPRC5B expression. Show less

The constitutive activity of melanocortin receptors (MCRs) is integral to several physiological processes. The unliganded cryo-electron microscopy structures of MC1R, MC2R, MC3R, MC4R, and MC5R in complex with G Show less

in the last decades, social networking sites (SNSs) use among adolescents has dramatically increased, feeding the adolescents' needs. However, younger users might be more vulnerable to problematic social networking. Scholar research increasingly highlighted the need to explore the underlying mechanisms of problematic use of SNSs. Difficulties in emotion regulation, general distress, experiences of shame, and specific motivations for SNSs use might represent risk factors for problematic social networking. On the contrary, other variables adolescence-related and potentially involved in problematic SNSs use (emptiness, boredom, emotional autonomy, and self-concept clarity) need further exploration. the present person-centered study aimed at profiling SNSs teen users (13-19 years) based on their (problematic) social networking, by comparing their SNSs-related behaviors and motivations, emotional dysregulation, distress symptoms, emptiness, boredom, shame, self-concept clarity, and emotional autonomy. the study involved 774 Italian adolescents (57% females; mean age = 15.74 ± 1.62 years) and four different profiles characterized by unique patterns of (problematic) social networking were identified through the latent profile analysis (LPA): (1) non-problematic SNSs users, (2) at-risk SNSs users, (3) problematic SNSs users, and (4) defended SNSs users (ntp=218; AIC=39125.44; BIC=39988.37; SSABIC=39296.00; entropy=.97; LMP-LRT p <.05; BLRT p <.05). concerning the emerging profiles, problematic and non-problematic SNSs users displayed the highest and lower levels of risk factors related to social networking, respectively. The so-called "Defended" profile might include participant adolescents who defensively avoided thinking about the psychological and emotional experiences of SNSs use, showing very low levels in all the variables exploring SNSs-related behaviors and motivations, and psychological risk. Show less

To explore the optimal row-ratio in mechanized hybrid rice seed production, a field experiment was conducted in 2024 at Qionglai and Mianzhu using 'Tiantai A' × 'Taihui 808'. Three row-ratio treatments (H1: 18:6, H2: 24:6, and H3: 30:6) were tested using agricultural unmanned aerial vehicles (AUAVs) for pollination assistance. The results showed that row-ratio had little effect on sterile line flowering dynamics. The index of flowers meeting (IFM) was 0.71-0.72 at Qionglai and 0.81-0.86 at Mianzhu, with 11 to 12 days of flowering duration. As the row-ratio increased, total pollen quantity in the panicle layer and grain filling rate (GFR) decreased, while grain infection rate (GIR) increased. The responses of grain blighted rate (GBR), grain empty rate (GER), and fertilization success rate (FSR) to row-ratio varied between sites. Pollen density and GFR followed the pattern of near region (NR) > central region (CR) > far region (FR). Within the panicle, pollen density was generally highest in the upper panicle layer (UPL), followed by the middle (MPL) and lower (LPL) layers, with partial exceptions observed in the H2 and H3 treatments at Mianzhu. The vertical distribution of GFR varied by site: at Qionglai, it was apical parts of panicle (APP) > median parts (MPP) > basal parts (BPP), whereas at Mianzhu the order was MPP > APP > BPP. With wider row-ratios, yield per unit area (YUA) and GFR declined (H1 > H2 > H3), while 1,000-grain weight increased or decreased and then increased. Under H1, yields reached 2,107.50 kg ha Show less

Essential tremor (ET) is a common neurodegenerative disorder characterized by action tremors and various non-motor symptoms. This study investigated the potential therapeutic effects of ketamine, an NMDA receptor antagonist with known GABA modulatory and anti-inflammatory properties, in a harmaline-induced model of ET in mice. We also evaluated the changes in expression of inflammatory interleukin 6 (IL-6) as well as Leucine rich repeat and Immunoglobin-like domain-containing protein 1 (Lingo-1), a prominent gene involved in the pathogenesis of ET. Male Swiss Webster mice were divided into four groups: control, harmaline (10 mg/kg), ketamine (8 mg/kg), and harmaline + ketamine. Tremor severity, muscle strength, locomotor activity, anxiety-like behavior, and passive avoidance learning were assessed. Cerebellar expression of Lingo-1 and IL-6 was analyzed using real-time PCR. Ketamine did not significantly reduce harmaline-induced tremors but improved muscle strength deficits in the wire grip test. In the open field test, ketamine normalized some harmaline-induced changes in locomotor activity and grooming behavior. No significant differences were observed in passive avoidance learning across groups. At the molecular level, ketamine did not mitigate the harmaline-induced increase in IL-6 expression, and Lingo-1 expression was not significantly altered by either harmaline or ketamine treatment. Our findings suggest that ketamine has limited efficacy in the harmaline ET model, showing some improvements in motor function and anxiety-like behavior but failing to address core tremor symptoms or modulate inflammatory and Lingo-1 pathways. These results highlight the complex nature of ET pathophysiology and the need for further research into targeted therapeutic approaches. Show less

Alzheimer's disease (AD) is a progressive neurodegenerative disorder with an unclear pathogenesis and no effective treatment methods. HY-021068 (HY), a novel class I drug, exhibits significant neuroprotective properties in ischemic brain injury. Recent studies suggest that neuronal ferroptosis may be a critical contributor to the onset and progression of AD. However, it is still unclear whether HY treatment has protective effects on AD by inhibiting ferroptosis. In this study, APP/PS1 double transgenic mice were used to investigate the effect and mechanism of HY in AD. In vitro, HT22 cells were stimulated with Amyloid β Show less

Examining how hypoglycemic medications affect brain function is one of the best approaches to addressing cognitive impairment. In this study, trelagliptin, a dipeptidyl peptidase-4 (DPP4) inhibitor, was utilized to assess memory loss in diabetic rats through fear conditioning tests. Trelagliptin restored fear memory in diabetic rats that had been disrupted over a relatively long period (24 h) or extended period (5 days). Moreover, trelagliptin treatment reduced the higher incidence of neuronal cell death in the cerebral cortex, as observed via Nissl or hematoxylin and eosin staining. Subsequent analyses revealed that diabetic rats exhibited elevated levels of inflammatory cytokines (p-IKKα and p-NFκB) and a trend toward oxidative damage, indicated by malondialdehyde (MDA), superoxide dismutase 2 (SOD2), and glutathione peroxidase 4 (GPX4) detection. However, administration of trelagliptin reversed these markers to baseline levels. Additionally, trelagliptin activated p-AMPK, p-AKT, and p-GSK-3β. Notably, trelagliptin upregulated the expression of postsynaptic density protein 95 (PSD95) and synaptotagmin 1 (SYT1) while downregulating amyloid precursor protein (APP) and beta-site amyloid precursor protein cleaving enzyme 1 (BACE1). These findings suggest that trelagliptin alleviates cognitive impairment in diabetic rats, likely through AMPK-AKT-GSK-3β-mediated mitigation of oxidative stress, enhancement of synaptic plasticity, and reduction of Aβ accumulation. Show less

Metabolic syndrome (MetS), a cluster of cardiometabolic abnormalities including elevated blood pressure, impaired glucose regulation, dyslipidemia, and increased waist circumference is increasingly recognized as a condition linked to both physical and psychological health risks. This study aims to investigate genotype-specific differences in psychological distress between healthy individuals and those with metabolic disorders, as well as to examine potential gene metabolic status interactions. This study is a cross-sectional analysis conducted in Turkistan city in the Southern region of Kazakhstan. Participants (healthy and those with metabolic syndrome) were invited to take part in the study by random sampling from the Khoja Akhmet Yassawi Kazakh-Turkish International University Medical Center. Consenting individuals provided a genetic analysis. Psychosomatic indicators were assessed using the Perceived Stress Questionnaire (PSQ) and the Depression, Anxiety, and Stress Scale (DASS-21). A total of 200 individuals participated, with an approximately 3:1 ratio of women to men. The mean age in years was 50.4 ± 9.5 and 48.8 ± 7.7 for men and women, respectively. Preliminary analyses showed variations in cognitive and psychosomatic measures among individuals with metabolic syndrome, but no associations with genetic variants, and no significant group differences across key psychosomatic indicators when stratified by metabolic or genetic factors. However, a significant difference in LPL-Anxiety between genotypes GA-GG ( Variations in metabolic and genetic factors within the studied population were not associated with measurable differences in stress or depressive symptoms. Show less

Little is known about the association between physical activity and the risk of pre-sarcopenic obesity (pre-SO) among adolescents. Hence, this study aimed to examine the association between physical activity and pre-SO in a sample of 2143 adolescents aged 12 to 18 years from Yinchuan, China. The pre-SO was defined by three criteria: low skeletal muscle mass adjusted by weight (SMM/W) combined with body mass index (BMI), fat mass percentage (FMP), and waist circumference (WC). After adjusting for age, smoking, drinking, sleep time, and high-fat food consumption, participants with high physical activity (HPA) had a lower risk of pre-SO compared to those with low physical activity (LPA) according to the obesity criteria of FMP (OR   0.63, 95% CI, 0.48-0.83, P < 0.05), and WC (OR 0.71, 95% CI, 0.52-0.96, P < 0.05). Additionally, restricted cubic spline models showed a linear dose-response association between total physical activity (TPA) and pre-SO no matter what obesity criteria were adopted (all P overall trend < 0.05, all P non-linear > 0.50). Subgroup analyses revealed that individuals with higher TPA levels exhibited a decreased risk of pre-SO in boys according to the obesity criteria of FMP, and WC. In conclusion, HPA is associated with a reduced risk of pre-SO in adolescents, especially among boys. Show less

GATA family transcription factors are somatically variable (SV) in esophageal adenocarcinomas (EAC) and inducible by simulated reflux. Our study examines the mechanisms whereby GATA family members (GATA4, GATA6, and the atypical TRPS-1) influence oncogenesis during the Barrett's esophagus (BE) metaplasia-dysplasia transition preceding EAC. RNAseq analyses of esophageal cell lines and lesion-derived adult stem cells (ASCs) in conjunction shRNA- or CRISPR-facilitated gene silencing, together with reanalysis of The Cancer Genome Atlas data, spatial transcriptomics, and organ-on-a-chip studies were used. Although a gastroesophageal reflux disease history positively correlated with GATA4/6 somatically variable and a columnar-associated gene signature (ANPEP/GATA4) in The Cancer Genome Atlas EAC cases, it negatively associated with a squamous lineage-linked signature (TP63/SOX15) containing TRPS1. In experimental data, opposing effects on regulators of squamous and columnar lineage identity were uncovered between TRPS1 and classical GATA factors (GATA4/6). Interrogation of this GATA "fulcrum" defined further genes (CGN, IL6R, and GPRC5B) targeted for TRPS1-mediated suppression or GATA4/6 activation. A novel spatial transcriptomic signature of BE-associated high-grade dysplasia (HGD) captured GATA fulcrum action, through GPRC5B expression. Functionally, GPRC5B was found to be low-pH-responsive, to increase proliferative and colony formation rates, and when overexpressed facilitate a hyperproliferative HGD-like transformation of BE-ASCs. Using an organ-on-a-chip platform, cellular overgrowth, reduced luminal villus structures, lower goblet cell numbers, and loss of intestine-associated marker gene expression (TFF3/MUC2) were observed following GPRC5B overexpression in BE-ASCs, mirroring HGD. This study identifies critical GATA factor-mediated processes underlying cellular phenotype in the BE-HGD-EAC transition and identifies GATA-inducible GPRC5B as a functional marker and possible driver of progression through HGD to EAC. Show less

Adipogenic differentiation of adipose-derived stem cells (ADSCs) is fundamental to both adipose tissue homeostasis and clinical applications, particularly fat grafting. However, the global and stage-specific transcriptional regulatory networks underlying ADSC adipogenesis remain incompletely elucidated. In this study, we integrated bulk and single-cell RNA-seq datasets across multiple time points of ADSC adipogenesis to identify core regulators of differentiation and maturation. A total of 41 genes were consistently upregulated during early differentiation, among which eight hub genes (FABP4, FASN, FABP5, ADIPOQ, PLIN1, LPL, CIDEC, and ACSL1) formed a tightly connected protein-protein interaction (PPI) module associated with lipid metabolism, lipid droplet formation, and adipocyte maturation. Further integration of differentially expressed lncRNAs and miRNAs led to the construction of a ceRNA network involving 7 mRNAs, 9 miRNAs, and 4 lncRNAs, comprising 34 predicted lncRNA-miRNA-mRNA regulatory axes. To identify temporal transcriptional regulators, we defined five genes (TTC14, MBNL2, UBR3, ABCD2, and SORT1) as early-stage inducers of adipogenesis, and four genes (UQCR11, NDUFB4, S100A10, and PRDX3) as late-stage regulators involved in maintaining the mature phenotype. These stage-specific regulators showed distinct temporal expression patterns and were validated by qPCR. GeneMANIA network analysis further revealed that early-stage regulators were enriched in lipid transport and lipase activity regulation, while late-stage regulators were associated with mitochondrial electron transport and energy metabolism. These findings highlight the stage-dependent transcriptional landscape of ADSC adipogenesis and provide candidate regulatory targets for modulating adipocyte differentiation and stability. Show less

The human genome is widely transcribed, with part of these transcribed regions producing stably expressed protein-coding or non-coding RNAs. Long intergenic non-coding RNAs (lincRNAs) are significantly differentially expressed in various cell lines and tissues. However, the influence of their transcription events remains unclear. In this study, we constructed a human genomic interaction network and found frequent interactions between lincRNA genes and protein-coding genes that are highly related to the occupancy of RNA polymerase II on the lincRNA gene. Interestingly, in the human genome interaction networks, the degree of lincRNA genes was significantly higher than that of protein-coding genes. The promoter regions of the protein-coding genes interacting with the lincRNA genes are enriched with R-loop structures, indicating that lincRNA may influence the target genes through R-loop structures. These promoters were enriched in more transcription factor binding sites. Furthermore, the whole network and sub-network could be utilized to explore potential biomarkers of leukemia. We found that zinc finger protein 668 (ZNF668), eosinophil granule ontogeny transcript (EGOT), and glutamate metabotropic receptor 7 (GRM7) could serve as novel biomarkers for acute myeloid leukemia (LMAL). Pasireotide acetate (CAS No. 396091-76-2) represents a potential drug for LMAL patients. These results suggested that potential biomarkers and corresponding drugs for cancer could be identified based on lincRNA-promoter network/sub-network topological parameters. Show less