Search Results (534)

Lipedema and obesity are often misdiagnosed or clinically confused yet arise via distinct mechanisms, complicating diagnosis and treatment. This review synthesizes evidence differentiating these conditions across genetic, hormonal, inflammatory and mechanical pathways to identify therapeutic targets. Lipedema may involve genetic predisposition (forkhead box C2 [FOXC2], prospero homeobox 1 [PROX1]), hormonal dysregulation with aberrant aromatase activity, and altered adipogenesis (peroxisome proliferator-activated receptor gamma [PPARγ], CCAAT/enhancer-binding protein [C/EBP]). A proinflammatory microenvironment with macrophage M1/M2 imbalance, elevated interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), and extracellular matrix remodeling is hypothesized to drive fibrosis. Emerging evidence implicates gut-derived endotoxemia (lipopolysaccharide [LPS]-toll-like receptor 4 [TLR4]-nuclear factor kappa-B [NF-κB]) and mechanotransduction (Yes-associated protein [YAP]/transcriptional coactivator with PDZ-binding motif [TAZ]) in adipocyte hypertrophy and treatment resistance. Obesity involves systemic metabolic dysfunction with visceral adiposity and cardiometabolic comorbidities. Lipedema patients maintain metabolic health, exhibit gluteofemoral fat distribution and experience neuropathic pain via nociceptor sensitization (transient receptor potential vanilloid 1 [TRPV1] and ankyrin 1 [TRPA1]) with central amplification. Weight-loss interventions are ineffective, necessitating targeted strategies. Promising targets include TLR4 antagonism, vascular endothelial growth factor C/vascular endothelial growth factor receptor-3 (VEGF-C/VEGFR3) modulation for lymphatic enhancement, YAP/TAZ inhibition and neuromodulators for pain. Physical therapy functions as a biological modifier targeting inflammation, lymphatic drainage and mechanotransduction. This review highlights promising but largely hypothesis-generating molecular insights and calls for validated biomarkers, rigorous clinical trials, and mechanism-based therapies. Many of the pathways discussed require further confirmation in human studies. Full article

In colorectal cancer (CRC), tumor progression is influenced by immunosuppressive tumor microenvironment (TME), in which innate immunity and adaptive immunity play an important role. CD47 is one of the key molecules in the process. It sends a “don’t eat me” signal to macrophages by binding to signal regulatory protein alpha (SIRPα), thus helping tumor cells escape immune clearance. Forkhead box P3 (FOXP3)⁺ regulatory immune cells further suppress antitumor T-cell responses. Here, based on a review of the literature and publicly available transcriptomic data, we propose that CD47 expression and FOXP3⁺ regulatory T cells in CRC are interconnected components of a broader myeloid–regulatory immunosuppressive phenotype, rather than a simple linear CD47–FOXP3 pathway. Evidence from cancer studies and exploratory GEPIA3/TIMER3.0 analyses supports a weak and method-dependent association between CD47 expression, FOXP3 transcripts, and estimated Treg infiltration. Hippo/Yes-associated protein/transcriptional coactivator with PDZ-binding motif (YAP/TAZ) signaling serves as a potential upstream program contributing to this immune context. Full article

Glioblastoma (GBM) is one of the most aggressive and treatment-resistant cancers, shaped by a tumor microenvironment (TME) that is both metabolically demanding and strongly immunosuppressive. GBM relies heavily on fatty acid (FA) metabolism to sustain growth of rapidly dividing tumor cells and survive metabolic stress. GBM cells enhance lipid uptake, activate sterol regulatory element-binding protein 1 (SREBP-1)-driven lipogenesis, store excess lipids in droplets to prevent toxicity, and depend on fatty acid oxidation (FAO) to generate adenosine triphosphate (ATP) and maintain redox balance, particularly under nutrient-limited conditions. GBM TME is also consistently enriched with regulatory T cells (Tregs), which maintain suppressive activity despite the nutrient restrictions that impair effector T cells (Teffs). In hypoxia and nutrient limitation within the TME, Tregs can adapt by using FAO, lactate oxidation, and OXPHOS, supported by forkhead box P3 (Foxp3)-dependent metabolic programming, cluster of differentiation 36 (CD36)-mediated FA uptake, and hypoxia-related signals. At the same time, programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) signaling reduces glycolytic activity in Teffs and contributes to metabolic dysfunction, while also supporting the stability of oxidative metabolism in Tregs. Evidence from pre-clinical and clinical studies suggests a possible association between Treg enrichment in GBM and reduced responsiveness to immune checkpoint inhibitors (ICIs), although this relationship is not yet fully defined. Overall, current findings point to FA metabolism as a shared metabolic axis that supports both tumor progression and Treg-mediated immune resistance. Targeting lipid-driven pathways may offer an opportunity to disrupt these advantages and improve the effectiveness of existing immunotherapies for GBM. Full article

Diabetes mellitus (DM) induces significant endocrine disruption and oxidative stress (OS) within the testes, resulting in impaired spermatogenesis, increased sperm abnormalities, and compromised reproductive function. This study aimed to evaluate the combined protective effects of Semaglutide (SEM) combined with Carica papaya (papaya) juice against type 2 diabetes-induced testicular damage in rats. Forty adult male albino rats were divided into four experimental groups: a control group, a Streptozotocin (STZ)-induced diabetic group, a diabetic group treated with SEM (0.3 mg/kg), and a diabetic group treated with SEM (0.3 mg/kg) in combination with 10% papaya juice, administered for eight weeks. Statistically significant superiority over SEM alone was observed for selected endpoints; the findings primarily support the potential of papaya as a dose-sparing adjunct rather than demonstrating uniformly enhanced efficacy. They significantly improved systemic metabolic parameters, as evidenced by reduced fasting blood glucose (FBG) and glycated hemoglobin (HbA_1c) levels and restoration of the lipid profile. Importantly, it also attenuated diabetes-induced testicular injury, as demonstrated by improved reproductive hormone levels, enhanced sperm parameters, restoration of antioxidant defenses, modulation of inflammatory and apoptotic signaling, and marked histopathological recovery of seminiferous tubular architecture. Antioxidant markers revealed a notable reduction in malondialdehyde (MDA) and cytochrome P450 2E1 (CYP2E1), along with significant increases in reduced glutathione, catalase (CAT), and superoxide dismutase (SOD). Furthermore, a marked modulation of key pro-inflammatory and pro-apoptotic mediators was observed, including forkhead box protein O1 (FOXO1), microRNA-155 (miR-155), tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B cell subunit 1 (NF-κB1), interleukin-6 (IL-6), caspase-3 (CASP3), and BCL2-Associated X Apoptosis Regulator (Bax), while a significant upregulation of sirtuin-1 (SIRT1), microRNA-34c (miR-34c), and B-cell lymphoma-2 (Bcl-2) was also detected. Histopathological assessments confirmed the restoration of normal testicular architecture in the treated groups. These findings indicate that the combination strategy may have the potential to achieve dose savings while maintaining efficacy comparable to the standard-dose SEM, through the enhancement of the antioxidant defenses, modulation of inflammation, and apoptosis, specifically via the modulation of the miR-34c/miR-155 and SIRT1/FOXO1 signaling. Full article

Estrogen receptor (ER)-positive breast cancer (BrCa) accounts for two-thirds of all BrCa cases worldwide. Therefore, ER-targeted endocrine therapy is the standard treatment for this disease. There has been a recent trend towards developing combination therapies using molecularly targeted drugs to improve outcomes. This study aimed to identify therapeutic targets demonstrating efficacy when combined with fulvestrant (a selective ER downregulator/degrader). We generated microRNA (miRNA) signatures from fulvestrant-treated MCF-7 cells by RNA sequencing. From the signature, we evaluated miR-374b-5p because its expression was elevated by fulvestrant treatment in MCF-7 cells. Also, in expression analysis by subtype of BrCa patients, miR-374b-5p expression was suppressed only in luminal BrCa. Ectopic expression assays revealed that miR-374b-5p attenuated the malignant phenotypes of MCF-7 cells. We searched for genes regulated by miR-374b-5p and discovered that 11 (NEK2, NUF2, HMMR, DEPDC1B, FOXM1, ELOVL6, KIF20A, NCAPH, CENPK, FAM83D, and KIAA0101) are closely involved in BrCa molecular pathogenesis. Among these target genes, we focused on forkhead box M1 (FOXM1), a transcription factor regulating cell cycle progression and division. Notably, combination therapy with fulvestrant and a FOXM1 inhibitor significantly suppressed MCF-7 cell proliferation. From the miRNA signature established in this study, we identified antitumor miR-374b-5p and its target genes and used these findings to explore candidate drugs with potential efficacy when combined with fulvestrant. Full article

Lifespan is increasing throughout the world leading to a rise in non-communicable diseases in the global population that impacts over 800 million individuals with metabolic disorders, such as diabetes mellitus. Metabolic disease presents a significant challenge for clinical care since multi-organ disease progression ensues despite a broad array of treatment protocols. The pursuit of innovative strategies with mammalian forkhead transcription factors of the “O” class (FoxOs) and intimately related pathways of aging, cellular senescence, telomere integrity, oxidative stress, programmed cell death with apoptosis, autophagy, ferroptosis, pyroptosis, and cuproptosis, Wnt/β-catenin signaling, Wnt1 inducible signaling pathway protein 1, and the gut microbiome becomes vital to address the clinical hurdles of metabolic disorders. Platforms incorporating novel diagnostics with artificial intelligence and machine learning can further address the underlying mechanisms tied to FoxOs that include the mechanistic target of rapamycin, AMP activated protein kinase, silent mating type information regulation 2 homolog 1 (S. cerevisiae), and glucagon-like peptide-1 receptor agonists that can markedly influence biological outcomes. Given the premise that it is essential to comprehend the intimate relationship that FoxO signaling pathways hold, FoxOs offer an exciting and promising approach to address the clinical aspects of disease onset, progression, and treatment with metabolic disorders. Full article

Objective: Impaired fatty acid oxidation (FAO) is considered an important metabolic mechanism underlying skeletal muscle aging and sarcopenia; however, the key regulatory molecules involved in this process remain incompletely defined. This study aimed to identify candidate biomarkers associated with impaired FAO in aged skeletal muscle, characterize their potential biological functions and regulatory features through integrated bioinformatics and machine learning analyses, and preliminarily validate their expression patterns in in vivo and in vitro aging models. Methods: Skeletal muscle aging transcriptomic datasets GSE1428 and GSE674 were obtained from the Gene Expression Omnibus database. FAO-related genes were retrieved from GeneCards. Differentially expressed FAO-related genes (DE-FAOGs) were identified through differential expression analysis and were further analyzed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. Random forest, Boruta, and protein–protein interaction (PPI) network analyses were used to screen hub genes, and an artificial neural network (ANN) model was constructed. Single-cell RNA sequencing analysis, gene set enrichment analysis, ceRNA network construction, drug prediction, molecular docking, and molecular dynamics simulation were further performed. Hub gene expression was validated by qRT-PCR in naturally aged mice and D-galactose-induced senescent C2C12 cells. Results: A total of 69 DE-FAOGs were identified and were mainly enriched in mitochondrial function, electron transport chain, and energy metabolism-related pathways. Three hub genes, creatine kinase, mitochondrial 2 (CKMT2), actin alpha cardiac muscle 1 (ACTC1), and forkhead box O3 (FOXO3), were identified by random forest, Boruta, and PPI analyses. Receiver operating characteristic (ROC) analysis showed good discriminatory performance for these genes. The three-gene ANN model achieved area under the curve (AUC) values of 0.992 and 0.964 in the training and validation datasets, respectively. Gene set enrichment analysis (GSEA) suggested that the hub genes were closely associated with mitochondrial energy metabolism, lipid metabolism, and stress regulation. qRT-PCR confirmed decreased Ckmt2 expression and increased Actc1 and Foxo3 expression under aging conditions, consistent with the bioinformatics results. Conclusions: CKMT2, ACTC1, and FOXO3 are potential biomarkers associated with impaired FAO in aged skeletal muscle. The ANN model based on these three genes showed good predictive performance and may provide new insights into the metabolic mechanisms and therapeutic targets of sarcopenia. Full article

Background and Objectives: Clear cell renal cell carcinoma (ccRCC) demonstrates substantial molecular and clinical heterogeneity, limiting the prognostic accuracy of conventional staging system and complicating treatment selection. CT-based radiomics and radiogenomics have emerged as promising non-invasive approaches for predicting molecular biomarkers. This review aimed to evaluate the current evidence regarding CT-based radiogenomics for the prediction of molecular markers in ccRCC, with emphasis on methodological approaches, predictive performance, and clinical applicability. Materials and Methods: A comprehensive literature search of PubMed/MEDLINE, Scopus, and Cochrane Library databases was performed for original studies published between January 2012 and December 2025. Eligible studies included patients with histopathologically confirmed ccRCC, performed CT-based radiomics feature extraction, and investigated molecular or genetic biomarkers using machine learning (ML) methods. Data regarding CT acquisition phase, segmentation strategy, radiomics features, ML algorithms, investigated biomarkers, and model performance metrics were extracted. Results and Discussion: Twenty-five retrospective studies were included. CT-based radiomics demonstrated promising performance in predicting gene mutations, including Von Hippel–Lindau (VHL), Polybromo 1 (PBRM1), BRCA1-associated protein 1 (BAP1), SET domain containing 2 (SETD2), and Lysine demethylase 5C (KDM5C), with reported area under the curve (AUC) values reaching 0.987. Radiogenomic models also showed utility in assessing hypoxia-related pathways, lipid metabolism signatures, programmed cell death profiles, immune-related markers, and tumor microenvironment characteristics, including programmed death-ligand 1 (PD-L1), Cluster of Differentiation 68 (CD68+) tumor-associated macrophages (TAMs), Cytotoxic T-Lymphocyte–Associated Protein 4 (CTLA-4), Forkhead Box P3 (FOXP3), and Ki-67 proliferation index. Predictive performance varied across biomarkers, with AUCs generally ranging from 0.68 to 0.91. Random Forest (RF), Logistic Regression (LR), Support Vector Machine (SVM), Adaptive Boosting (AdaBoost), and Gradient Boosting algorithms were most commonly applied. Conclusions: CT-based radiogenomics represents a promising non-invasive tool for molecular characterization and risk stratification in ccRCC. Standardized multicenter prospective studies, methodological homogeneity, and external validation are required before routine clinical implementation. Full article

Gastric cancer is a multifactorial disease characterized by complex interactions among transcriptional regulation, inflammation, metabolic adaptation, and angiogenesis. However, systemic molecular relationships linking these processes remain insufficiently understood. This study aimed to evaluate circulating levels of FOXA2 (Forkhead Box A2), Ang-1 (Angiopoietin-1), ApoE4 (Apolipoprotein E4), PEN-2 (Presenilin Enhancer-2), and NF-κB (Nuclear Factor kappa B) in gastric cancer patients and to explore their potential integrated role in disease biology. Serum samples were obtained from 40 patients with gastric cancer (20 preoperative and 20 postoperative) and 20 healthy controls. Protein levels were measured using enzyme-linked immunosorbent assay (ELISA), followed by statistical analysis. Serum levels of FOXA2, ApoE4, PEN-2, and NF-κB were significantly decreased in gastric cancer patients compared with healthy controls, whereas Ang-1 levels were significantly increased. No statistically significant differences were observed between preoperative and postoperative groups. These findings indicate coordinated dysregulation of transcriptional, inflammatory, metabolic, and angiogenic processes in gastric cancer. The identified FOXA2–NF-κB–PEN-2–ApoE4–Ang-1 axis may be considered an integrated circulating molecular profile reflecting tumor host interactions and may provide a potential foundation for future non-invasive biomarker development and translational research. This study proposes systems-level circulating molecular network model rather than isolated biomarker alterations. Full article

(1) Background: Reactive oxygen species (ROS) act as physiological signaling mediators but contribute to oxidative damage, cellular dysfunction, and age-related disease when redox homeostasis fails. Forkhead box O4 (FOXO4) has emerged as a redox-sensitive regulator linking stress adaptation, antioxidant defense, and cellular senescence. This structured narrative review critically evaluates which redox- and aging-related conclusions are supported directly for FOXO4 and which remain inferred from other FOXO isoforms. (2) Methods: PubMed/MEDLINE, Scopus, and Web of Science were searched from inception to May 2026; Google Scholar was used only for supplementary citation tracking and did not contribute a separate platform-level count. Of 420 records, 300 remained after deduplication, 110 full texts were assessed, and 89 publications were retained. FOXO4-related evidence was classified as directly FOXO4-specific (n = 18), FOXO-family/conserved (n = 24), or extrapolated predominantly from FOXO1/FOXO3/DAF-16 (n = 20); 27 contextual publications on redox biology, senescence, disease, and NRF2 were tracked separately. (3) Results: The strongest FOXO4-specific evidence supports three mechanistic axes: cysteine-dependent redox sensing, stress-regulated nuclear trafficking and coactivator engagement through transportin-1 and p300/CBP, and FOXO4–p53-mediated survival of senescent cells. By contrast, direct FOXO4 regulation of commonly cited antioxidant targets, including SOD2, catalase, sestrins, and GADD45, remains insufficiently demonstrated and is inferred mainly from FOXO3 or broader FOXO-family studies. FOXO4-DRI has shown senolytic activity in preclinical models, including vascular endothelium, but has not been clinically validated. (4) Conclusions: FOXO4 is a redox-responsive transcriptional regulator with well-supported roles in cysteine-based signaling and senescent-cell survival, whereas its target-gene-level antioxidant program remains incompletely resolved. Clinical translation of FOXO4–p53 disruption requires isoform- and tissue-specific validation, pharmacokinetic and delivery studies, long-term toxicology, and explicit assessment of p53-dependent tumor surveillance. Full article

Forkhead box O (FoxO) transcription factors act downstream of insulin signaling and play conserved roles in development and metabolic homeostasis in insects. However, whether FoxO participates in 20-hydroxyecdysone (20E)-mediated pupation and fat body remodeling in honeybee larvae remains unclear. Here, we show that FoxO is highly expressed during the prepupal and pupal stages of honeybee development. RNA interference (RNAi)-mediated silencing of FoxO delayed pupation, inhibited ecdysteroid biosynthesis and 20E signaling, and ultimately led to pupal lethality. Knockdown of FoxO also suppressed the expression of lipolytic genes, reduced lipase activity, and increased triglyceride (TG) accumulation in the fat body. Furthermore, FoxO deficiency impaired autophagy, as evidenced by reduced LysoTracker staining, decreased autophagosome formation, and downregulation of Atg genes. These findings demonstrate that FoxO participates in 20E-induced pupation of honeybee by regulating the expression of key genes involved in 20E biosynthesis and the 20E signaling pathway. FoxO coordinates autophagy and lipid mobilization in the fat body to provide energy for pupal development. Collectively, our results establish FoxO as a central regulator linking endocrine signaling, energy metabolism, and tissue remodeling during honeybee metamorphosis. Full article

Autoimmune endocrine diseases constitute a group of disorders characterized by immune-mediated destruction or dysfunction of hormone-producing glands. The pathogenesis of these diseases reflects a breakdown of immune tolerance in which regulatory T cells (Tregs) play a key role. The transcription factor forkhead box P3 (FOXP3) is a master regulator of Treg differentiation and suppressive function. Also, it is central to maintaining self-tolerance. Genetic mutations in FOXP3, including those responsible for immune dysregulation, polyendocrinopathy, enteropathy X-linked (IPEX) syndrome, highlight the critical role of FOXP3 in endocrine immune tolerance. Emerging evidence suggests that autoimmune endocrine disorders may reflect organ-specific destabilization of FOXP3 expression rather than complete Treg deficiency. The reversibility or irreversible loss of FOXP3 gene expression represents a key determinant of Treg plasticity and the persistence of autoimmune inflammation. This review proposes an integrated genetic–epigenetic model of FOXP3 instability and examines how the endocrine microenvironment shapes Treg plasticity. Genetic or epigenetic alterations affecting FOXP3 expression can impair Treg activity and precipitate endocrine organ-specific autoimmunity. Epigenetic mechanisms such as DNA methylation, histone modifications, and non-coding RNA-mediated regulation that modulate FOXP3 transcriptional activity are discussed. From a translational perspective, the potential of FOXP3 as a biomarker for endocrine disease susceptibility and progression was summarized. Furthermore, therapeutic strategies employed for expanding or engineering functional FOXP3⁺ Tregs using antigen-specific vaccines, chimeric antigen receptors (CAR)-Tregs, gene therapy, or low-dose interleukin-2 (IL-2) were described. Full article

Colorectal cancer (CRC) is intricately linked to gut microbiota dysbiosis and tryptophan (Trp) metabolic dysregulation. This study aimed to clarify the role and mechanisms of 20(S/R)-ginsenoside Rh1 in suppressing colorectal cancer through the regulation of gut microbiota and Trp metabolism. Azoxymethane/dextran sulfate sodium (AOM/DSS)was employed to induce a CRC mouse model, followed by treatment with 20(S/R)-ginsenoside Rh1 at 100 mg·kg⁻¹·day⁻¹ for 6 weeks. 20(S/R)-ginsenoside Rh1 significantly reduced the disease activity index (DAI) score, restored colon length, and decreased tumor count. 20(S/R)-Ginsenoside Rh1 ameliorated gut dysbiosis by increasing gut microbial diversity and elevating the prevalence of beneficial bacteria, including Lactobacillus, and stimulated the production of indole derivatives, including indole-3-propionic acid (IPA), indole-3-acetic acid (IAA), and indole-3-lactic acid (ILA) by enriching Trp -metabolizing bacteria such as Lactobacillus reuteri. These changes further activated the AhR/CYP1A1/IL-22 and PXR/TLR4 pathways, upregulated the expression of intestinal tight junction proteins, suppressed the secretion of proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and IFN-γ, and elevated the levels of the anti-inflammatory cytokine IL-10. Furthermore, 20(S/R)-ginsenoside Rh1 reduces the serum kynurenine (Kyn)/Trp ratio, downregulates the expression of forkhead box P3 (FoxP3), a marker of regulatory T (Treg) cells, and increases the number of CD8⁺ T cells by inhibiting the expression of indoleamine 2,3-dioxygenase 1 (IDO1) in colonic tissue. In conclusion, 20(S/R)-ginsenoside Rh1 showed potential anti-CRC activity, with our study observing links between its action and gut microbiota structure regulation, Trp metabolism modulation, AhR/PXR-mediated intestinal barrier activation, and IDO1-related immune suppression reversal. Full article

Therapy resistance remains a major obstacle to successful cancer treatment and is driven by complex interactions between tumor-intrinsic adaptive mechanisms and signals originating from the tumor microenvironment. Among the molecular regulators implicated in these processes, the transcription factor FOXM1 has emerged as a key mediator of DNA damage repair, cell cycle progression, and stress adaptation. Although FOXM1 has traditionally been studied as a regulator of intracellular signaling pathways, accumulating evidence suggests that its functions extend beyond canonical transcriptional control. In this review, we analyze current knowledge on the mechanisms regulating FOXM1 expression and activity and discuss how FOXM1 contributes to therapy resistance. We propose that FOXM1 should be viewed not merely as a regulator of individual oncogenic pathways but as a systems-level coordinator that integrates intracellular stress adaptation with microenvironment-driven resistance mechanisms. Particular attention is given to the FOXM1 interactome, complemented by an analysis of protein interaction data from BioGRID. We also discuss emerging evidence implicating FOXM1 in intercellular communication. To identify potential links between FOXM1 signaling and extracellular vesicle cargo, we analyzed the overlap between FOXM1 target genes and proteins identified in extracellular vesicle proteome databases. These emerging regulatory networks may represent previously underappreciated contributors to therapy resistance. Full article

Tuberculosis (TB) remains a major global public health burden. This study aimed to identify differentially expressed messenger RNAs (mRNAs) and circulating microRNAs (miRNAs) associated with TB and to validate their potential roles in the disease. We performed RNA sequencing (RNA-Seq) on peripheral blood samples from 10 patients with active pulmonary TB and 10 healthy controls, using peripheral blood mononuclear cells (PBMCs) for mRNA sequencing and plasma for miRNA sequencing. Given the exploratory nature of the plasma miRNA data and the limitations of the U6 normalization method, the results for circulating miRNAs will need to be validated using alternative methods in subsequent experiments. A total of 1323 differentially expressed mRNAs and 49 differentially expressed miRNAs were identified. Functional annotation of differentially expressed genes was conducted using the Database for Annotation, Visualization and Integrated Discovery (DAVID), followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, which revealed two TB-associated pathways: “MicroRNAs in cancer” and “Small cell lung cancer.” Two key mRNAs—tumor protein p53 (TP53) and forkhead box protein P1 (FOXP1)—and one key miRNA (hsa-miR-29b-3p) were identified as potential core regulatory factors. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) validation confirmed that the expression patterns of these candidate molecules were consistent with the RNA-Seq results. Three potential candidate molecules associated with TB were ultimately identified, although their disease specificity remains to be determined. Full article