Search Results (105)

Endometriosis is a hormone-dependent disease, in the pathophysiology of which sex hormones (androgens, estrogens, etc.) are involved. The level of bioactive androgens/estrogens (in the free state) in the organism largely depends on sex hormone-binding globulin (SHBG), which binds/transports a significant portion of the androgens/estrogens of the body and, due to this, changes the amount of these hormones in a free state (bioactive), which may be important in the development of endometriosis. The study was devoted to identifying the link between the genetic determinants (single nucleotide polymorphisms [SNPs]) of SHBG (according to predating genome-wide associative studies [GWAS]) and the risk of endometriosis in the Caucasian women of Russia. The study was accomplished on a total sample of 1368 women (395 endometriosis; 973 endometriosis free [controls]). Nine loci with an impact on SHBG level in predating GWAS have been examined. The search for associations of these loci with endometriosis was carried out: both their independent effects and interlocus interactions with an in silico interpretation of the functionality/pathways in which endometriosis-related loci and strongly linked SNPs were involved have been evaluated. Polymorphic locus rs440837 (A > G) ZBTB10 correlated with endometriosis development (recessive genetic model): the SHBG-raising genotype GG rs440837 (A > G) ZBTB10 serves as a risk factor for the disease formation; its presence in the genotype almost doubles the risk of endometriosis (OR = 1.91; 95%CI = 1.13–2.98; p_perm = 0.024; power = 81.13%). The SHBG-impacts of 7 SNPs from 9 analyzed loci such as rs17496332 (A > G) PRMT6, rs780093 (C > T) GCKR, rs10454142 (T > C) PPP1R21, rs3779195 (T > A) BAIAP2L1, rs440837 (A > G) ZBTB10, rs7910927 (G > T) JMJD1C, and rs8023580 (T > C) NR2F2 interacting with each other have been endometriosis-associated. Endometriosis-causal SNP rs440837 (A > G) ZBTB10 and 5 proxy SNPs determine the DNA interaction in the region of 3 genes (RP11-48B3.3, RP11-48B3.4, ZBTB10) with 22 transcription factors and, due to this, affect the processes of development of the endocrine system, gene transcription regulation, TGF-beta signaling pathway, regulation of cell proliferation/differentiation, etc. In conclusion, the results of this study showed the endometriosis risk effect of the SHBG-impact polymorphic variants. Full article

Dental pulp tissue, enclosed within rigid dentin, is susceptible to bacterial invasion via dentinal tubules, often leading to severe pulpal inflammation. This condition is typically associated with a hypoxic microenvironment, yet the mechanistic link between hypoxia and inflammation remains unclear. We identified a marked upregulation of microRNA-210 (miR-210) in human dental pulp cells (hDPCs) cultured under hypoxic conditions. This study investigated the role of miR-210 in modulating inflammation in lipopolysaccharide (LPS)-stimulated hDPCs. Hypoxic conditions and enforced expression of hypoxia-inducible factor 1α (HIF1α) significantly increased miR-210 levels. While LPS stimulation elevated proinflammatory cytokines (Interleukin-6, Monocyte Chemoattractant Protein-1, and Tumor Necrosis Factor Alpha) and activated nuclear factor-kappa B (NF-κB) signaling, miR-210 overexpression suppressed LPS-mediated cytokine production and NF-κB activity. Luciferase assays revealed that miR-210 targets and negatively regulates TGF-beta activated kinase 1 binding protein 1 (TAB1), a key upstream regulator of NF-κB. Transfection with an miR-210 mimic reduced TAB1 expression, NF-κB activation, and cytokine output in both LPS-stimulated hDPCs and rat pulp tissue ex vivo. Conversely, miR-210 inhibition enhanced TAB1 levels and inflammatory cytokine expression under hypoxic conditions. These findings suggest that miR-210 mitigates inflammation via the TAB1–NF-κB pathway, functioning as a negative feedback regulator. miR-210 may represent a promising therapeutic target for pulpal inflammation. Full article

Soyasaponin intolerance is common in ancient fish species, making them susceptible to enteritis caused by dietary soybean meal. β,β-Dimethylacrylshikonin is the key active monomer found in Lithospermum erythrorhizon and is known for its multiple pharmacological activities. However, its effect on soybean meal-induced enteritis remains unknown. The administration of 2 g/kg of β,β-Dimethylacrylshikonin (LE) effectively alleviated 5 g/kg of soyasaponin-induced histopathological changes and dysfunction, as evidenced by the expression of inflammation-related genes (il-1β, il-8, and il10). Regarding the gut microbiota composition, LE therapy decreased the population of inflammation-linked Proteobacteria and concurrently elevated the proportion of Fusobacteriota, effectively sustaining the balance of the zebrafish gut microbiota. Moreover, at the genus level, LE treatment also increased the abundance of Cetobacterium. Transcriptional results suggested that LE intervention mainly regulated immune-related pathways, including cytokine–cytokine receptor interaction, the TGF-beta signaling pathway, taurine and hypotaurine metabolism, and arachidonic acid metabolism. In conclusion, 5 g/kg of soyasaponins caused intestinal injury in zebrafish, and β,β-Dimethylacrylshikonin can reduce intestinal inflammation by regulating the intestinal microbial balance and metabolic disorder, with the best effect at 2 g/kg. Full article

Phase separation is one of the mechanisms critical for protein function, and its aberrances are associated with cancer development. However, mutations that affect protein phase separation and cancer development have not been systematically identified and analyzed. In this study, we systematically identified the mutations affecting protein liquid–liquid phase separation in multiple cancers. We calculated the phase separation scores alterations for over 1,200,000 mutations across 16 cancer types using the TCGA dataset. We then performed pathway enrichment, kinase, TF enrichment, and survival analysis to identify related biological processes and clinical implications. Nearly 10% of the mutations were defined to affect phase separation in pan-cancer. These mutations occupied a consistent percentage in each cancer type. Extremely influencing mutations accumulate on stomach adenocarcinoma (STAD), uterine corpus endometrial carcinoma (UCEC), and skin cutaneous melanoma (SKCM). Moreover, proteins carrying these mutations are enriched in cancer-related pathways, including TGF-beta signaling pathways and polycomb repressive complex. Phase separation of these proteins would be regulated by kinases, including CDK1, CDK2, and EGFR, and transcription factors, including ZNF407, ZNF318, and MGA proteins, to play functions in cancer. Protein–Protein Interaction Network revealed that these phase separation proteins are highly interconnected. Finally, patients carrying mutations that positively affect the protein phase separation are associated with poor prognosis in skin cutaneous melanoma (SKCM) and lung squamous cell carcinoma (LUSC), which could be partially explained by the pathogenicity of these mutations. The study provided a pan-cancer landscape for depicting the association of phase separation and cancer mutations, which would be a rich data resource for understanding the association of cancer mutations and phase separation. Full article

Emery–Dreifuss muscular dystrophy (EDMD) is caused by mutations in EMD, LMNA, SYNE1, SYNE2, and other related genes. The disease is characterized by joint contractures, muscle weakening and wasting, and heart conduction defects associated with dilated cardiomyopathy. Previous studies demonstrated the activation of fibrogenic molecules such as TGFbeta 2 and CTGF in preclinical models of EDMD2 and increased secretion of TGFbeta 2 in patient serum. A wide screening of patient cells suggested fibrosis, metabolism, and myogenic signaling as the most affected pathways in various EDMD forms. In this study, we show that alpha-smooth muscle actin-positive myofibroblasts are overrepresented in patient fibroblast cultures carrying EMD, LMNA, or SYNE2 mutations, and profibrotic miRNA-21 is upregulated. Upon CRISPR/Cas correction of the mutated EMD or LMNA sequence in EDMD1 or EDMD2 fibroblasts, respectively, we observe a reduced expression of fibrogenic molecules. However, in patient myoblasts, neither fibrogenic proteins nor miRNA-21 were upregulated; instead, miRNA-21-5p was downregulated along with muscle-specific miRNA-133b and miRNA-206, which have a crucial role in muscle cell homeostasis. These observations suggest that the conversion of laminopathic fibroblasts into a profibrotic phenotype is a determinant of EDMD-associated muscle fibrosis, while miRNA-206-dependent defects of laminopathic myoblasts, including altered regulation of VEGF levels, contribute to muscle cell deterioration. Notably, our study provides a proof-of-principle for the application of gene correction to EDMD1 and EDMD2 and presents EDMD1 isogenic cells that exhibit an almost complete rescue of a disease-specific miRNA signature. These cells can be used as experimental models for studying muscular laminopathies. Full article

Polyphenols play a crucial role in promoting human health. This study aims to investigate the polyphenols of black hulless barley bran (HBP) and evaluate their anti-diabetic mechanisms in vivo. Using UPLC-QTOF-MS/MS, 27 compounds were identified in HBP, including four phenolic acids, 14 flavonoids, and nine anthocyanidins. High contents of Chrysoeriol 7-O-glucuronide (42.09 mg/g), Cyanidin 3-O-glucoside (21.02 mg/g), and Cyanidin 3-O-(6″-O-malonyl)-glucoside (24.45 mg/g) were quantified via UPLC in HBP. Administration of HBP significantly reduced fasting blood glucose (FBG), improved glucose intolerance and lipid profiles, and alleviated liver and pancreatic damage in type 2 diabetic (T2DM) mice. Furthermore, it enhanced serum antioxidant enzyme activities and modulated inflammatory cytokines. Transcriptomic analysis revealed that HBP influenced signal transduction and the immune system, particularly in key signaling pathways, including Hippo, TGF-beta, HIF-1, and p53, associated with T2DM. Although HBP had minimal impact on gut microbiota diversity and SCFA levels, it presents a promising candidate for T2DM intervention through its multifaceted mechanisms. Full article

Background/Objectives: Colorectal cancer (CRC) is one of the most common malignancies worldwide. microRNAs (miRNAs) are small non-coding RNA molecules that regulate gene expression post-transcriptionally and have emerged as important regulators in cancer biology. This study aimed to investigate the roles of miR-379-5p and miR-519a-3p in CRC using Quantitative Real-Time PCR (RT-qPCR) and comprehensive bioinformatic analyses. Methods: Tumor tissues and matched adjacent normal tissues were collected from 54 patients with CRC. The expression levels of miR-379-5p and miR-519a-3p in these tissues were determined using the RT-qPCR method. To investigate the functional roles of differently expressed miRNAs, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to construct miRNA–transcription factor (TF)–target gene–disease interaction networks. Results: It was found that the expression level of miR-379-5p was statistically significantly increased in tumor tissues compared to normal tissues, while miR-519a-3p was decreased (p < 0.05). GO analysis revealed enrichment in several important biological processes, including cellular protein metabolic processes, biosynthetic processes, response to stress, and nucleic acid binding TF activity. KEGG analysis exhibited that dysregulated miRNAs were associated with important pathways related to carcinogenesis, such as p53 signaling, TGF-beta signaling, and FoxO signaling pathways. Additionally, the miRNAs-TFs-Genes-Diseases Networks analysis identified ESR1 and FOXA1 as common target TFs of dysregulated miRNAs. Network analyses showed that dysregulated miRNAs interact with CRC-associated genes (Caspase 3 (CASP3), Adenomatous polyposis coli (APC), and AKT serine/threonine kinase 3 (AKT3)). Conclusions: The present study indicates that miR-379-5p and miR-519a-3p may be involved in CRC progression, with miR-379-5p being upregulated and miR-519a-3p being downregulated in tumor tissues. However, further functional studies are required to clarify their potential roles in tumor biology. The findings of the study suggest that miR-379-5p and miR-519a-3p may be associated with regulatory pathways related to CRC. These miRNAs have the potential to serve as diagnostic biomarkers or therapeutic targets in CRC. Full article

Basal-like breast cancer (BLBC) is associated with poor prognosis, high recurrence rates, and limited therapeutic options, largely due to its molecular heterogeneity and complexity, which include epigenetic alterations. This study investigated epigenetic regulatory networks in BLBC by analyzing DNA methylation in distal cis-regulatory regions and its impact on genes, transcription factors (TFs), and microRNAs (miRNAs) expression. Data from TCGA were processed using the ELMER and DESeq2 tools to identify differentially methylated regions and differentially expressed genes, TFs, and miRNAs. The FANMOD algorithm was used to identify the regulatory interactions uncovering the feed-forward loops (FFLs). The analysis identified 110 TF-mediated FFLs, 43 miRNA-mediated FFLs, and five composite FFLs, involving 18 hypermethylated and 32 hypomethylated genes, eight upregulated and nine downregulated TFs, and 21 upregulated and seven downregulated miRNAs. The TF-mediated FFLs major regulators involved the AR, EBF1, FOS, FOXM1, and TEAD4 TFs, while key miRNAs were miR-3662, miR-429, and miR-4434. Enriched pathways involved cAMP, ErbB, FoxO, p53, TGF-beta, Rap1, and Ras signaling. Differences in hallmark gene set categories reflected distinct methylation and miRNA expression profiles. Overall, this integrative analysis mapped the intricate epigenetic landscape of BLBC, emphasizing the role of FFLs as regulatory motifs that integrate DNA methylation, TFs, and miRNAs in orchestrating disease’s development and progression and offering potential targets for future diagnostic and therapeutic strategies. Full article

Background: Colorectal cancer (CRC) is strongly influenced by miRNAs as well as the circadian system. Methods: High-throughput sequencing of miRNAs expressed in the rat colon during 24 h light (L)/dark (D) cycle was performed to identify rhythmically expressed miRNAs. The role of miR-150-5p in CRC progression was analyzed in DLD1 cell line and human CRC tissues. Results: Nearly 10% of mature miRNAs showed a daily rhythm in expression. A peak of miRNAs’ levels was in most cases observed during the first half of the D phase of the LD cycle. The highest amplitude was detected in expression of miR-150-5p and miR-142-3p. In the L phase of the LD cycle, the maximum in miR-30d-5p expression was detected. Gene ontology enrichment analysis revealed that genes interfering with miRNAs with peak expression during the D phase influence apoptosis, angiogenesis, the immune system, and EGF and TGF-beta signaling. Rhythm in miR-150-5p, miR-142-3p, and miR-30d-5p expression was confirmed by real-time PCR. Oncogenes bcl2 and myb and clock gene cry1 were identified as miR-150-5p targets. miR-150-5p administration promoted camptothecin-induced apoptosis. Expression of myb showed a rhythmic profile in DLD1 cells with inverted acrophase with respect to miR-150-5p. miR-150-5p was decreased in cancer compared to adjacent tissue in CRC patients. Decrease in miR-150-5p was age dependent. Older patients with lower expression of miR-150-5p and higher expression of cry1 showed worse survival in comparison with younger patients. Conclusions: miRNA signaling differs between the L and D phases of the LD cycle. miR-150-5p, targeting myb, bcl2, and cry1, can influence CRC progression in a phase-dependent manner. Full article

Isoforms of prostate transmembrane protein, androgen induced 1 (PMEPA1), are regulated either by TGF-beta or AR activation and provide negative loop-regulation of these signaling pathways. High levels of PMEPA1 protein have been observed in various tumor types, including prostate, bladder, colorectal cancers, and glioblastoma. Direct oncogenic role of PMEPA1 in hepatocellular carcinoma has been recently shown on an animal model. New studies also indicate an upregulation of PMEPA1 in tumor-associated immune and stromal cells; however, its specific role in tumor stromal cells remains largely unexplored. In our previous research, we developed a cancer-stroma sphere (CSS) model that integrates tumor cells with mesenchymal stem cells (MSCs). Evaluations of chemotherapy and CAR-T therapies on CSSs have demonstrated that this model closely mimics in vivo data regarding cytotoxicity and adverse effects of therapy. In the present study, we reveal that PMEPA1 is significantly overexpressed in MSCs within the CSS. Moreover, this overexpression has been induced under short-term co-culture conditions. Among the five isoforms of PMEPA1, PMEPA1a and PMEPA1b isoforms have been detected in MSCs. These findings underscore the potential role of PMEPA1 in the tumor microenvironment modulation by MSCs. Full article

Background: Head and neck cancer (HNC) remains a global health challenge with a poor 5-year survival rate among patients with relapsed or advanced-stage disease. Immune checkpoint blockade therapies have emerged as a promising approach to improve outcomes; however, their effectiveness is limited, with response rates of only 15–20% because of immune evasion mechanisms. MicroRNA (miRNA) dysregulation plays a key role in facilitating such immune evasion. In this study, we aim to identify specific miRNAs whose altered expression contributes to immune escape in HNC. Methods: We employed an integrated bioinformatics approach, incorporating differential expression analysis, survival analysis, target prediction, KEGG immune pathway analysis, a protein–protein interaction network, and the identification of hub genes using in silico tools. Results: Our analysis revealed that a high expression of miR-18a and miR-2355 was associated with reduced survival, with the median survival decreasing from 42.9 to 27.8 months, respectively, in advanced-stage patients. Conversely, a low expression of let-7c and miR-6510 was linked to poor prognosis, with survival decreasing from 40.1 to 19.2 months and from 50.1 to 26.8 months, respectively, across disease progression. Further pathway analysis revealed that these miRNAs are significantly involved in the regulation of key immune evasion signaling pathways, including T cell receptor, PD-L1/PD-1 checkpoint, JAK-STAT, TGF-beta, NF-kappa B, and TNF signaling pathways. Hub gene analysis identified AKT1, STAT3, NFKB1, CD4, IL2RB, TLR4, and CTLA-4 as potential dysregulated miRNA targets, with enrichment in immune-related signaling pathways. Conclusions: Taken together, these findings suggest that targeting these miRNAs could modulate immune evasion mechanisms and potentially enhance the efficacy of ICB therapies in HNC. Full article

Introduction: Early-onset colorectal cancer (EOCRC) is rising rapidly, particularly among the Hispanic/Latino (H/L) populations, who face disproportionately poor outcomes. The transforming growth factor-beta (TGF-β) signaling pathway plays a critical role in colorectal cancer (CRC) progression by mediating epithelial-to-mesenchymal transition (EMT), immune evasion, and metastasis. However, integrative analyses linking TGF-β alterations to clinical features remain limited—particularly for diverse populations—hindering translational research and the development of precision therapies. To address this gap, we developed AI-HOPE-TGFbeta (Artificial Intelligence agent for High-Optimization and Precision Medicine focused on TGF-β), the first conversational artificial intelligence (AI) agent designed to explore TGF-β dysregulation in CRC by integrating harmonized clinical and genomic data via natural language queries. Methods: AI-HOPE-TGFbeta utilizes a large language model (LLM), Large Language Model Meta AI 3 (LLaMA 3), a natural language-to-code interpreter, and a bioinformatics backend to automate statistical workflows. Tailored for TGF-β pathway analysis, the platform enables real-time cohort stratification and hypothesis testing using harmonized datasets from the cBio Cancer Genomics Portal (cBioPortal). It supports mutation frequency comparisons, odds ratio testing, Kaplan–Meier survival analysis, and subgroup evaluations across race/ethnicity, microsatellite instability (MSI) status, tumor stage, treatment exposure, and age. The platform was validated by replicating findings on the SMAD4, TGFBR2, and BMPR1A mutations in EOCRC. Exploratory queries were conducted to examine novel associations with clinical outcomes in H/L populations. Results: AI-HOPE-TGFbeta successfully recapitulated established associations, including worse survival in SMAD4-mutant EOCRC patients treated with FOLFOX (fluorouracil, leucovorin and oxaliplatin) (p = 0.0001) and better outcomes in early-stage TGFBR2-mutated CRC patients (p = 0.00001). It revealed potential population-specific enrichment of BMPR1A mutations in H/L patients (OR = 2.63; p = 0.052) and uncovered MSI-specific survival benefits among SMAD4-mutated patients (p = 0.00001). Exploratory analysis showed better outcomes in SMAD2-mutant primary tumors vs. metastatic cases (p = 0.0010) and confirmed the feasibility of disaggregated ethnicity-based queries for TGFBR1 mutations, despite small sample sizes. These findings underscore the platform’s capacity to detect both known and emerging clinical–genomic patterns in CRC. Conclusions: AI-HOPE-TGFbeta introduces a new paradigm in cancer bioinformatics by enabling natural language-driven, real-time integration of genomic and clinical data specific to TGF-β pathway alterations in CRC. The platform democratizes complex analyses, supports disparity-focused investigation, and reveals clinically actionable insights in underserved populations, such as H/L EOCRC patients. As a first-of-its-kind system studying TGF-β, AI-HOPE-TGFbeta holds strong promise for advancing equitable precision oncology and accelerating translational discovery in the CRC TGF-β pathway. Full article

Sheep have evolved remarkable phenotypic diversity through artificial and natural selection, with reproductive traits being pivotal for breeding economics. As a unique genetic resource, Pishan red sheep exhibit exceptional advantages, including perennial estrus, high fecundity, and stable hereditary characteristics, establishing them as an optimal model for investigating reproductive genetics. In this study, we performed whole-genome resequencing of Pishan red sheep, generating 9084.81 Gb of raw data and identifying 53,968,686 high-quality single-nucleotide polymorphisms (SNPs). Through selective sweep analysis, 92 genomic regions under selection were detected, containing 90 positional candidate genes significantly associated with growth, reproduction, and immune functions. Notably, we revealed BMPRIB, UNC5C, PDLIM5, GRID2, and HPGDS as core positional candidate genes influencing litter size, operating through the TGF-beta and Thyroid hormone signaling pathways. A genome-wide association study (GWAS) further identified 59 trait-related SNPs, including 39 loci linked to growth traits (affecting positional candidate genes such as PROM1, TAPT1, LDB2, and KIF16B) and 20 loci of positional candidate genes associated with reproductive traits (involving ASPA, RAP1GAP2, PHIP, and WDR82).These findings not only elucidate the molecular basis of superior reproductive performance in Pishan red sheep, but also provide functional markers for precision breeding. Full article

Tumor cells and the tumor microenvironment (TME) produce factors, including neurotrophins, that induce axonogenesis and neurogenesis, and increase local nerve density. Proliferative growing cancer cell clusters and disseminated invasive tumor cells undergoing partial epithelial-to-mesenchymal transition (pEMT) can invade peripheral nerves. In the early stages of tumor–nerve interactions, Schwann cells (SCs) dedifferentiate, become activated and migrate to cancer cell nests; later, they induce pEMT in tumor cells and activate tumor cell migration along nerves. The SC–tumor–nerve interaction attracts myeloid-derived suppressor cells (MDSCs) and inflammatory monocytes, and the latter differentiate into macrophages. SCs and MDSCs are responsible for the activation of transforming growth factor-beta (TGF-beta) signaling. Intra-tumoral innervation is followed by perineural invasion (PNI), which has an unfavorable prognosis. What are the interventional options against PNI: local reduction in tumor nerves or inhibition of TGF-beta-related events, inhibition of downstream signaling of TGF-beta or immune activation, or intervention against immunosuppression? This systematic review is based on the Prisma 2009 search method and provides an overview of tumor–nerve interaction. Full article

Geese (Anser cygnoides) are popular worldwide with consumers for their unique meat quality, egg production, foie gras, and goose down; however, the key genes that influence geese growth remain elusive. To explore the mechanism of geese growth, a total of 500 Zhedong White geese were raised; four high-weight (HW) and four low-weight (LW) male geese were selected to collect carcass traits and for further transcriptomic and metabolomic analysis. The body weight and average daily gain of HW geese were significantly higher than those of the LW geese (p-value < 0.05), and the yields of the liver, gizzard, glandular stomach, and pancreas showed no significant difference between the HW and the LW group (p-value > 0.05). Compared with the LW geese, 19 differentially expressed genes (DEGs) (i.e., COL11A2, COL22A1, and TF) were detected in the breast muscle from the HW geese, which were involved in the PPAR signaling pathway, adipocytokine signaling pathway, fatty acid biosynthesis, and ferroptosis. A total of 59 differential accumulation metabolites (DAMs), which influence the pathways of glutathione metabolism and vitamin B6 metabolism, were detected in the breast muscle between the HW and LW geese. In the liver, 106 DEGs (i.e., THSD4, CREB3L3, and CNST) and 202 DAMs were found in the livers of the HW and LW groups, respectively. DEGs regulated the pathways of the TGF-beta signaling pathway, pyruvate metabolism, and adipocytokine signaling pathway; DAMs were involved in pyrimidine metabolism, nitrogen metabolism, and phenylalanine metabolism. Correlation analysis between the top DEGs and DAMs revealed that in the breast muscle, the expression levels of COL11A2 and COL22A1 were positively correlated with the content of S-(2-Hydroxy-3-buten-1-yl)glutathione. In the liver, the expression of THSD4 was positively correlated with the content of 2-Hydroxyhexadecanoic acid. In addition, one DEG (LOC106049048) and four DAMs (mogrol, brassidic acid, flabelline, and L-Leucyl-L-alanine) were shared in the breast muscle and liver. These important results contribute to improving the knowledge of goose growth and exploring the effective molecular markers that could be adopted for Zhedong White goose breeding. Full article