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PubMed2025

Prenatal pyrethroid exposure, placental gene network modules, and neonatal neurobehavior.

Prenatal pesticide exposure may adversely affect child neurodevelopment which may partly arise from impairing the placenta's vital role in fetal development. In a cohort of pregnant farmworkers from Thailand (N = 248), we examined the links between urinary metabolites of pyrethroid pesticides during pregnancy, placental gene expression networks derived from transcriptome sequencing, and newborn neurobehavior assessed using the NICU Network Neurobehavioral Scales (NNNS) at 5 weeks of age. Focusing on the 21 gene network modules in the placenta identified by Weighted Gene Co-expression Network Analysis, our analysis revealed significant associations between metabolites and nine distinct modules, and between thirteen modules and NNNS, with eight modules showing overlap. Notably, stress was negatively associated with the interferon alpha response and Myc target modules, and the interferon alpha response module was correlated positively with attention, and negatively with arousal, and quality of movement. The analysis also highlighted the early and late trimesters as critical periods for the exposures influence on placental function, with pyrethroid metabolites measured early in pregnancy significantly negatively associated with the protein secretion module, and those measured later in pregnancy negatively associated with modules related to oxidative phosphorylation (OXPHOS) and DNA repair. Additionally, the cumulative sum of 3-phenoxybenzoic acid across pregnancy was significantly negatively associated with the OXPHOS module. These findings suggest that prenatal exposure to pyrethroids may influence neonatal neurobehavior through specific placental mechanisms that impact gene expression of metabolic pathways, and these effects may be pregnancy period specific. These results offer valuable insights for future risk assessment and intervention strategies.

Prenatal Exposure Delayed Effects↗

PubMed2026

The 100 Diatom Genomes Project.

One hundred diatom species have been selected for genome and transcriptome sequencing. The 100 Diatom Genomes Project aims to provide a scalable framework for understanding diatom biodiversity, ecology and evolution, and for investigating their use in biotechnology.

Diatoms↗

PubMed2026

Therapeutic effect and anti-inflammatory mechanism of modified Shoutai pills against lipopolysaccharide-induced miscarriage in mice.

OBJECTIVE: To elucidate the anti-inflammatory mechanisms of modified Shoutai pills (, MSTP) in miscarriages, we performed transcriptome sequencing on the decidua and placental tissues of pregnancy mice. METHODS: The therapeutic effects and anti-inflammatory mechanisms of MSTP were studied in mice with lipopolysaccharide (LPS)-induced miscarriage. First, the effects of MSTP on pregnancy outcomes and the maternal-fetal interface, in LPS-induced miscarriage mice were examined. RNA sequencing was used to further investigate gene expression changes in LPS-induced miscarriage mice and to assess the effects of MSTP intervention. Finally, the expression levels of inflammation-related genes in the decidua and placental tissues were determined using quantitative real-time polymerase chain reaction (qRT-PCR). RESULTS: A high dose of MSTP significantly decreased the resorption rate (P < 0.05) and reduced apoptosis of the decidua and placental tissues in mice. Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses showed that inflammatory and immune-related signals were enriched. qRT-PCR results confirmed that in decidual and placental tissues, MSTP reduced the gene expression levels of toll-like receptor 4 (TLR4), nuclear factor kappa-B (NF-κB), c-Jun N-terminal kinase 1, p38, and tumor necrosis factor-α. CONCLUSIONS: In this study, we demonstrated that MSTP effectively prevented embryo loss with an anti-inflammatory mechanism through downregulation of the TLR4-NF-κB/ MAPK signaling pathway, in LPS-induced miscarriage mice model. To our knowledge, this is the first study to reveal the therapeutic mechanism of MSTP in LPS-induced miscarriage in mice.

Animals↗

PubMed2026

Genomic Characterization of ETV6::RUNX1-Positive Childhood B-ALL in a Chinese Cohort: Novel Fusion Partners, Co-Occurring Mutations, and Risk-Stratifying Biomarkers.

BACKGROUND: ETV6::RUNX1 is the most common genetic abnormality in pediatric B-cell acute lymphoblastic leukemia (ALL; ∼25%), yet the comprehensive genetic architecture and molecular predictors of intermediate-risk (IR) stratification remain incompletely characterized. METHODS: We performed whole-transcriptome sequencing (Illumina NovaSeq 6000, rRNA depletion, 41.70 Gb/sample) on bone marrow samples from 93 pediatric ETV6::RUNX1-positive B-ALL patients. Bioinformatics analysis included STAR alignment, MuTect2 variant calling, FusionCatcher fusion detection, and VEP annotation. The Jaccard index with permutation testing assessed mutation co-occurrence; logistic regression identified independent predictors of IR classification. RESULTS: Beyond ETV6::RUNX1, we identified 51 distinct fusion genes across the cohort, including the reciprocal RUNX1-ETV6 (73.1%), chr8::KLF1210 (38.7%), and KLF12-chr8 (34.4%). Somatic mutations in 249 genes were detected; the most frequent were KIAA1715 (17.2%), KRAS (11.8%), and NSD2 (10.8%). Network analysis revealed significant chromatin modifier co-occurrence (KIAA1715-KMT2C: J = 0.136, p = 0.015) and KRAS-NRAS mutual exclusivity (J = 0.000, p = 0.042). PTCH1 (OR = 3.50, 95% CI 0.21-58.49, p = 0.41) and GNB1 (OR = 6.5, 95% CI 1.2-34.8, p = 0.029) mutations independently predicted IR classification. chr8::KLF1210 fusion correlated with higher Day-19 MRD levels (p = 0.038). CONCLUSIONS: GNB1 mutation represents a novel independent predictor of IR stratification in ETV6::RUNX1-positive B-ALL. The chromatin modifier co-occurrence module and extensive fusion architecture reveal biological heterogeneity within this favorable-risk subtype, with potential implications for risk-adapted therapeutic strategies.

B‐ALL↗

PubMed2026

Tripterygium Glycosides Alleviates Hemophagocytic Lymphohistiocytosis Accompanied With Aggressive NK Cell Leukemia and Epstein-Barr Virus Infection.

Hemophagocytic lymphohistiocytosis (HLH) is a group of hyperinflammatory disorders with a mortality rate exceeding 50%. We report a case of a female Asian patient who developed secondary HLH accompanied by aggressive natural killer cell leukemia and Epstein-Barr virus (EBV) infection, and was treated with tripterygium glycosides (TG), a Chinese patent medicine. Within 3 weeks of oral administration, the patient's recurrent high fever resolved, abdominal distension and splenomegaly improved, ascites diminished, serum soluble CD25 levels decreased, and hematopoietic and coagulation functions recovered. Triptolide, a major component of TG, exhibited cytotoxicity against the patient's ascitic cells and induced apoptosis in a dose-dependent manner ex vivo. Whole-genome and transcriptome sequencing of the patient's tumor cells revealed that TG regulated EBV-associated mutated genes such as PSMD7 and modulated inflammation-related pathways. Molecular docking further suggested direct targeting of PSMD7 by triptolide. Tripterygium glycosides quickly mitigated cytokine storm, alleviated symptoms of HLH, and showed no observed adverse effects with a good cost-benefit profile, thereby offering a potential bridge for follow-up hematopoietic stem cell transplantation.

Humans↗

PubMed2026

Multimodal features and prognostic risk assessment in locally advanced gastric cancer patients following neoadjuvant therapy based on machine learning algorithms: a multicenter study.

BACKGROUND: Neoadjuvant therapy (NAT) is recommended for locally advanced gastric cancer (LAGC), but some patients respond poorly. We aimed to construct a multimodal model integrating CT images, transcriptomic sequencing, and clinicopathological data to assess prognosis in LAGC patients receiving NAT. MATERIALS AND METHODS: This multicenter study included 505 LAGC patients who underwent NAT. Radiomic features were extracted from preoperative CT images of 505 patients. RNA-seq was performed on 277 post-NAT specimens, with additional data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases (n = 804). Patients were divided into training (168 cases), internal validation (72 cases), and external validation cohorts. Machine learning algorithms identified key radiomic, molecular, and clinical features associated with NAT response, which were then integrated into a multimodal model to predict overall survival (OS) and disease-free survival (DFS). RESULTS: Six radiomic and three molecular features significantly associated with NAT response were selected. Radiomic risk (hazard ratio [HR]: 4.0, P < 0.001) and molecular risk (HR: 7.1, P < 0.001) were independent prognostic factors. By integrating radiomic risk, molecular risk, and clinical characteristics, a multimodal model (MuMo) was constructed.The C-index results (OS, C-index = 0.855; DFS, C-index = 0.786) demonstrated that MuMo outperformed the single-modality models and ypTNM staging.Mechanistic analysis suggested that the efficacy of neoadjuvant therapy was significantly enriched in immune-inflammatory pathways. CONCLUSIONS: MuMo can effectively predict postoperative survival risk in LAGC patients receiving NAT, serving as a powerful tool for optimizing prognostic assessment.

Humans↗

PubMed2025

Comprehensive investigation identifies CPSF3 as a novel prognostic and oncogenic biomarker in bladder cancer.

BACKGROUND: Bladder cancer (BC) remains a prevalent malignancy worldwide, with rising incidence rates each year. Despite progress in therapeutic strategies, many patients suffer recurrence or progression, emphasizing the urgent need for novel prognostic biomarkers and therapeutic targets. This research evaluated the prognostic relevance and functional role of Cleavage and Polyadenylation Specificity Factor 3 (CPSF3) in BC. METHODS: We analyzed CPSF3 expression using The Cancer Genome Atlas data and immunohistochemistry on a cohort of 203 BC patients. A nomogram incorporating CPSF3 expression was developed based on CPSF3 expression for prediction of overall survival and disease-free survival. Immune infiltration analyses and transcriptome sequencing were performed to explore underlying biological mechanisms. In vitro and in vivo experiments were utilized to examine the results of CPSF3 silencing on bladder cancer cell growth, colony-forming ability and cell cycle transitions. RESULTS: Elevated CPSF3 expression was significantly linked to unfavorable overall survival and disease-free survival both in TCGA datasets and our cohort. The CPSF3-based nomogram outperformed conventional prognostic models. CPSF3 expression was associated with tumor-infiltrating immune cells and immune checkpoint markers. Enrichment analysis revealed CPSF3 enrichment in cell cycle-related pathways. Suppression of CPSF3 expression led to marked reductions in cell proliferation, colony formation, tumor growth in animal models and inhibited G1 to S phase progression. CONCLUSION: CPSF3 is a promising prognostic biomarker for BC and may play a crucial role in BC progression. Incorporating CPSF3 into clinical prognostic models may enhance prediction of patient outcomes. CPSF3 may represent a promising therapeutic target for BC management.

Bladder cancer↗

PubMed2026

AKR7A3 rs1738023 association with susceptibility to female hepatocellular carcinoma and its role in AFB1 metabolism and tumor.

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common cancer worldwide. In this study, we performed a two-stage exome-chip association analysis and found that the aldo-keto reductase family7 member A3 (AKR7A3) rs1738023 may be a potential susceptibility locus for HCC in females. We aimed to explore its role and mechanism. METHODS: The association between genotype and phenotype was analyzed through GWAS method. The expression of AKR7A3 in cancer tissue and blood analysis by qRT-PCR. The relationship of AKR7A3 and aflatoxin B1 (AFB1) was also analyzed. The effect of AKR7A3 on the biological behavior of HCC cell line was investigated on proliferation and invasion. The potential mechanism was analyzed by transcriptome analysis and western blot. RESULTS: Through genome-wide association analysis (GWAS), AKR7A3 (rs1738023), KIF2C (rs4342887), and CYP3A5 (rs6977165 and rs4646450) were found to be associated with susceptibility to hepatocellular carcinoma (HCC) in women. Further expression quantitative trait loci (eQTL) analysis showed that only AKR7A3 (rs1738023) was significantly associated with gene expression. The expression of AKR7A3 was significantly lower in HCC than adjacent non-tumorous tissues (P < 0.001). The genotype of rs1738023 was significantly associated with AKR7A3 expression (P = 0.0085). Rs1738023[C] genotype had a low AKR7A3 expression level and limited detoxification ability of AFB1. Literature data showed that AKR7A3 is involved in the metabolism of aflatoxin B1 (AFB1). Functional experimental results showed that overexpression of AKR7A3 in the normal liver cell line HL-7702 could significantly reduce AFB1-induced ROS levels and DNA adduct formation, suggesting that it plays a protective role in AFB1 metabolic detoxification. Cell function test showed that overexpression of AKR7A3 inhibit the proliferation, migration and invasion of HCC cells, and block the cell cycle. Transcriptome sequencing and KEGG pathway enrichment analysis revealed that overexpression of AKR7A3 affected the PI3K signaling pathway and led to downregulation of HIF1A and its downstream VEGFA protein expression. The validation results were confirmed in HCC cell lines Huh-7 and SUN-387. CONCLUSION: Overexpression of AKR7A3 contributes to inhibition of HCC progression and reduction of aflatoxin toxicity. AKR7A3 may serve as a potential prognostic and therapeutic target for HCC patients, although further validation is needed.

AKR7A3↗

PubMed2026

Functional role and regulatory network of miR-22-3p in chicken hepatic lipid metabolism.

Although microRNA-22-3p (miR-22-3p) is abundantly expressed in the avian liver, its epigenetic role in lipid homeostasis remains largely uncharacterized. To elucidate its in vivo function, 14-day-old female Qingyuan Partridge chickens were intravenously injected with lentiviral vectors to establish miR-22-3p overexpression and knockdown models. Phenotypic analysis demonstrated that miR-22-3p knockdown significantly elevated hepatic triglyceride (TG) levels (p < 0.05) and drove marked steatosis, whereas its overexpression reduced TG content. Transcriptome sequencing (RNA-Seq) revealed profound metabolic remodeling, identifying 23 core lipid-associated genes (e.g., ELOVL6, FADS2, ACSBG2, and PTGIS) heavily enriched in steroid biosynthesis, fatty acid metabolism, and elongation pathways. In conclusion, miR-22-3p functions as a bidirectional epigenetic rheostat that negatively regulates hepatic lipid deposition by orchestrating a multilayered polygenic network, providing novel molecular targets for mitigating avian metabolic disorders and optimizing production traits in indigenous poultry breeds.

Animals↗

PubMed2026

Toxicological effects of propyl 4-hydroxybenzoate on gallstone pathogenesis: An integrated mendelian randomization, network toxicology, and experimental study.

BACKGROUND: Gallstone disease is a prevalent digestive disorder with substantial global socioeconomic burden. Propyl 4-hydroxybenzoate (PP), a widely used paraben preservative, exhibits potential metabolic and hepatic toxicity, yet its role in gallstone pathogenesis remains unclear. This study aimed to explore the causal association between PP exposure and gallstone formation and the underlying mechanism. METHODS: Two-sample Mendelian randomization (MR) was performed using genome-wide association study (GWAS) data. Network toxicology, molecular docking, and molecular dynamics simulation were applied to screen for core targets. In vivo experiments, transcriptome sequencing, Western blot (WB), and ELISA were conducted for mechanistic validation. RESULTS: MR confirmed a causal link between circulating PP levels and an elevated risk of gallstones (P < 0.05), with AKT1 identified as the key target. In mice, PP aggravated gallstone formation by activating the AKT1-NF-κB-CXCL1 pathway, enhancing hepatic inflammation and neutrophil extracellular traps (NETs) formation; these effects were reversed by AKT inhibition. CONCLUSION: PP promotes gallstone formation via the AKT1-NF-κB-CXCL1-NETs axis. Our findings highlight PP as an environmental risk factor for gallstones, providing novel insights into their prevention and targeted therapy.

Animals↗

PubMed2026

Luteolin is associated with alleviation of cigarette smoke-induced cellular senescence and inflammation in mice involving the CREB/c-Fos/NQO1 pathway.

Cigarette smoke (CS) exposure is a major risk factor for chronic obstructive pulmonary disease (COPD) and is closely associated with cellular senescence. Previous studies have demonstrated the efficacy of luteolin in treating aging-related symptoms. This study aims to elucidate the therapeutic potential of luteolin against CS-induced cellular senescence. Using a CS-exposed mouse model and cigarette smoke extract (CSE) treated mouse lung epithelial cells (TC-1), we demonstrate that luteolin significantly attenuates CS-induced histopathological alterations and inflammatory cytokine release while alleviating cellular senescence. Transcriptome sequencing suggests that NQO1 and Fos may serve as a common molecular target for both CS-induced pathology and luteolin treatment. Subsequent Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Set Enrichment Analysis (GSEA) enrichment analysis and pathway validation experiments revealed that the cAMP agonist Forskolin inhibits senescence marker expression by activating the CREB pathway, exhibiting a mechanism similar to that of luteolin. Notably, luteolin activation of this pathway may not depend on PKA activation. Ultimately, the study found that luteolin mitigates inflammatory responses and prevents lung epithelial cell senescence via the CREB/c-Fos/NQO1 pathway. These findings not only suggest the pivotal role of NQO1 in regulating CS-induced cellular senescence but also underscore the potential of luteolin as a therapeutic drug.

Animals↗

PubMed2025

Genomic insights into the population history of fat-tailed sheep and identification of two mutations that contribute to fat tail adipogenesis.

INTRODUCTION: Since their domestication, domestic sheep (Ovis aries) have been culturally and economically significant farming animals worldwide. Fat-tailed sheep serve as a unique genetic resource for understanding adipogenesis and adaptive evolution in livestock. OBJECTIVES: Several genomic analyses have been conducted on various sheep breeds to elucidate the genome and regulation mechanism of the fat tail trait, prior genomic studies have failed to reconcile conflicting evidence about the genetic basis of tail morphology, particularly regarding the roles of PDGFD and BMP2. METHODS: Here, we conducted whole-genome resequencing of 283 sheep, encompassing 66 domestic breeds and 5 wild ovine species, to investigate the domestication history and selection signatures of fat-tailed sheep. Additionally, we performed transcriptome sequencing on adipose tissue to identify differentially expressed genes and cellular assays to validate these results. RESULTS: Demographic analysis revealed that domestic sheep descended from Asiatic mouflon and fat-tailed sheep began to diverge from thin-tailed sheep approximately 4.4-7.5 thousand years ago in East Asia. Chinese indigenous sheep were classified into Mongolian, Kazakh, Tibetan, and Yunnan populations. The Yunnan population may have experienced more recent genetic introgression from wild species, rather than an independent domestication event. Moreover, many potential regions associated with the fat-tailed phenotype (DDI1, PDGFD, and BMP2) were identified by selective sweep and genome-wide association analyses. Additionally, a fine-scale analysis of fat-tailed and thin-tailed sheep revealed two novel mutations: a G/A missense variant of PDGFD (Chr15: 3900312) and a C/T missense variant of BMP2 (Chr13: 48462350), both of which were significantly associated with tail adiposity. Functional validation demonstrated that mutant A-PDGFD significantly activated PFGFD expression and reduced fat deposition compared to wildtype. The C-BMP2 mutant activated BMP2 expression and promoted preadipocyte fat deposition. CONCLUSION: Our study provides the first evidence that these genes jointly regulate fat tail development through complementary mechanisms: PDGFD promotes adipose expansion, whereas BMP2 modulates energy partitioning. These findings offer new insights into the evolutionary history of fat-tailed sheep and identify potential targets for precision breeding in small ruminants.

Animals↗

PubMed2025

Heme oxygenase 1 (HO-1) is a drug target for reversing cisplatin resistance in non-small cell lung cancer.

INTRODUCTION: Platinum-based drugs, the most widely used chemotherapeutic drugs in clinical oncology, have long faced the problem of drug resistance, which is urgently in need of resolution. Identifying biomarkers of drug resistance may help reduce platinum resistance and improve therapeutic efficacy. OBJECTIVES: This study aims to identify potential biomarkers associated with the development of cisplatin resistance in non-small cell lung cancer (NSCLC) and explore mechanisms to overcome chemoresistance. METHODS: NSCLC cisplatin resistance cell lines were constructed, and transcriptome sequencing was performed. Results were validated using Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. Molecular docking, proteomics sequencing, and in vitro and in vivo experiments were conducted to evaluate the role of Heme Oxygenase 1 (HO-1) in cisplatin resistance. RESULTS: NSCLC cisplatin resistance cell lines, GEO and TCGA data identified HMOX1, downstream of Nrf2, as a key drug resistance gene induced by cisplatin. Activation of the Nrf2/HO-1 pathway was found to induce ferroptosis resistance, a critical mechanism of cisplatin resistance. Candidate compounds SB 202190 and Nordihydroguaiaretic acid (NDGA) effectively reactivated ferroptosis by inhibiting HO-1, thereby increasing cisplatin sensitivity. CONCLUSION: The Nrf2/HO-1 pathway is a significant contributor to cisplatin resistance in NSCLC. Targeting HO-1 with SB 202190 and NDGA presents a promising strategy to overcome resistance and improve chemotherapy outcomes.

Cisplatin↗

PubMed2025

Cetobacterium somerae ZNN-1 promotes goblet cell differentiation through glutamine-mediated Notch signaling suppression.

INTRODUCTION: The gut microbiota acts as a crucial mediator in the interaction between the diet components and the host metabolism. However, the molecular mechanism by which the gut microbiota adapts to dietary components and subsequently regulates host physiological responses remains unclear. OBJECTIVES: This study aimed to investigate the response of gut microbiota to a plant-based protein diet (soybean meal, SM) and the effects of gut microbiota on host intestinal barrier function, along with the underlying mechanisms in a fish model. METHODS: Histopathological examination, and transepithelial electrical resistance test were used to evaluate the effects of Cetobacterium somerae on intestinal barrier function. Potential molecular mechanisms were validated by integrating whole-genome sequencing, microbiota composition sequencing, transcriptomics, and metabolomics, and utilizing in vitro cell models and mouse-derived organoid models. RESULTS: The results revealed that the SM diet significantly increased the abundance of Cetobacterium somerae in fish. Administration of C.somerae ZNN-1, a dominant strain isolated from the intestine of fish fed with the SM diet, enhanced the intestinal barrier function, particularly increasing the number of goblet cells in the intestine. Whole genome analysis of C. somerae ZNN-1 showed carbohydrate metabolism-associated genes were the most abundant in its metabolic modules. C.somerae ZNN-1 supplementation significantly inhibited the Notch signaling pathway in fish intestine. Metabolomics analysis revealed that administration of C.somerae ZNN-1 increased the glutamine level in fish gut. In vitro experiments demonstrated that glutamine regulated the differentiation of goblet cell by inhibiting the Notch signaling pathway in both human intestinal epithelial cell model and mouse intestinal organoid model. CONCLUSION: C. somerae served as a key bacterium adapted to soybean meal-derived carbohydrates, and it promoted goblet cell differentiation by inhibiting the Notch pathway. This study provides a new perspective for unraveling the interaction mechanisms among diet components, intestinal microbiota and host health.

Animals↗

PubMed2026

Functional identification of the key gene Eh-fadB in nicosulfuron degradation by Enterobacter hormaechei ES1 based on multi-omics and enzymatic characterization.

Nicosulfuron is a sulfonylurea herbicide with residues that pose ecological risks in agricultural soils. Here we elucidated the degradation mechanism of Enterobacter hormaechei ES1 through whole-genome sequencing, transcriptomics, metabolomics, gene knockout, heterologous expression, and soil bioremediation assays. Under nicosulfuron stress, ES1 upregulated antioxidant enzymes including SOD, POD, and CAT, along with glutathione synthesis, to scavenge excess reactive oxygen species. HPLC-TOF-MS identified degradation intermediates such as ADMP and ASDM, indicating initial cleavage of the sulfonylurea bridge. Integrated multi-omics prioritized Eh-fadB, encoding a fatty acid β-oxidation multifunctional enzyme, as a novel degradative gene. Targeted knockout of Eh-fadB reduced nicosulfuron degradation from 87.6% to 37.04%, while genetic complementation restored nearly full activity. Purified Eh-FadB directly converted nicosulfuron, with optimal performance at 30 °C and pH 5-6; its activity was enhanced by Na+ and Pb2+ but inhibited by Fe3+. Molecular docking and dynamics identified His-450 and Asn-427 as key residues for substrate binding. In contaminated soil, inoculation with ES1 reduced nicosulfuron content within 21 days and promoted recovery of dehydrogenase and urease activities. This study provides the first genetic and biochemical evidence that a FadB-type enzyme participates in nicosulfuron catabolism, supporting sulfonylurea bridge cleavage and its potential for soil bioremediation.

Eh-fadB↗

PubMed2026

Long-day photoperiod promotes growth of pea (Pisum sativum L.) via auxin biosynthesis and polar transport.

Photoperiodic sensitivity is an essential factor that may affect agricultural practices under current climate scenarios. This study used pea (Pisum sativum) to examine effects of varying photoperiods on growth and photosynthetic parameters and then reveal the mechanistic basis of this process by linking them with tissue-specific distribution of auxin and regulation of related genes. This was achieved by transcriptome sequencing, genome-wide gene family identification, and expression pattern analysis. Best results in terms of growth and yield were obtained with a 20 h/4 h light/dark photoperiod and these plants had the highest content of endogenous indole-3-acetic acid (IAA) in both the shoot apex and the root. Genes consistently upregulated with prolonged light exposure were significantly enriched in pathways related to light signal transduction, photosynthetic carbon metabolism, and phytohormone signal transduction. Through genome-wide identification, we characterized the TAA/TAR and YUCCA families (key gene families involved in auxin biosynthesis) as well as the PIN family (responsible for auxin polar transport) in pea. Extending the light duration positively affected expression of several genes related to auxin biosynthesis and transport, among them members of the Elongated Hypocotyl (HY) and Phytochrome-Interacting Factor (PIF) families being key light-induced transcription factors, PsTAR2, the principal gene regulating auxin biosynthesis, as well as PsPIN4, PsPIN5, PsPIN11, and PsPIN13 which mediate polar auxin transport. By elucidating mechanisms underlying the coordinated regulation of pea growth by light and auxin, this work provides a significant reference for photoperiod research on long-day crops for both protected- and field-based horticulture.

Auxin↗

PubMed2025

Nanobioreactor detection of space-associated hematopoietic stem and progenitor cell aging.

Human hematopoietic stem and progenitor cell (HSPC) fitness declines following exposure to stressors that reduce survival, dormancy, telomere maintenance, and self-renewal, thereby accelerating aging. While previous National Aeronautics and Space Administration (NASA) research revealed immune dysfunction in low-earth orbit (LEO), the impact of spaceflight on human HSPC aging had not been studied. To study HSPC aging, our NASA-supported Integrated Space Stem Cell Orbital Research (ISSCOR) team developed bone marrow niche nanobioreactors with lentiviral bicistronic fluorescent, ubiquitination-based cell-cycle indicator (FUCCI2BL) reporter for real-time HSPC tracking in artificial intelligence (AI)-driven CubeLabs. In month-long International Space Station (ISS) missions (SpX-24, SpX-25, SpX-26, and SpX-27) compared with ground controls, FUCCI2BL reporter, whole-genome and transcriptome sequencing, and cytokine arrays demonstrated cell-cycle, inflammatory cytokine, mitochondrial gene, human repetitive element, and apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3 (APOBEC3) deregulation together with clonal hematopoietic mutations. Furthermore, HSPC functionally organized multi-omics aging (HSPC-FOMA) analyses revealed reduced telomere maintenance, adenosine deaminase acting on RNA1 (ADAR1) p150 self-renewal gene expression, and replating capacity indicative of space-associated HSPC aging that may limit long-duration spaceflight.

Humans↗

PubMed2026

HIF-1 signaling contributes to lenvatinib resistance in patient-derived HCC organoids.

Resistance to lenvatinib remains an important limitation in hepatocellular carcinoma treatment. Six patient-derived organoid lines were established and classified as sensitive or resistant according to ex vivo drug responses, retaining histological and immunophenotypic features of matched parental tumors. Resistant organoids showed unchanged ATP activity, whereas sensitive ones exhibited pronounced morphological changes and reduced ATP activity at higher concentrations. Transcriptome sequencing identified 408 upregulated and 269 downregulated genes in resistant versus sensitive organoids, with HIF-1 signaling among altered pathways. In resistant organoids, lenvatinib increased HIF-1α, ANGPT2, and HK3 mRNA, whereas comparable changes were not detected in sensitive organoids. KC7F2 reduced these transcripts and further decreased ATP activity when combined with lenvatinib. In organoid-derived xenografts, this combination suppressed tumor growth and HIF-1 target expression more than lenvatinib alone, indicating HIF-1 signaling contributes to the resistant phenotype and its inhibition may enhance response.

Drug resistance↗