Biomedical subjects

Hong Yu

Publications and source records attributed to Hong Yu.

6 recordsLinked to original sources

PubMed2026

DEK::AFF2 Fusion-Associated Sinonasal Carcinoma With Intracranial and Orbital Involvement.

Sinonasal carcinomas encompass a molecularly heterogeneous group of malignancies. DEK::AFF2 fusion-associated carcinoma is a recently recognized subtype of nonkeratinizing squamous cell carcinoma characterized by deceptively bland morphology yet clinically aggressive behavior. We report the case of a 67-year-old woman who presented with a rapidly enlarging sinonasal mass with extensive local invasion involving both the intracranial compartment and orbit. Histologically, the tumor was composed of cytologically bland cells with monotonous nuclei and exhibited a combination of exophytic and endophytic growth patterns that closely mimicked a sinonasal papilloma. Although the tumor shows predominantly squamous differentiation, focal extracellular mucin was also present. The brain-invasive foci demonstrated tumor cells in sheets and nests floating within pools of mucin, a pattern focally reminiscent of mucinous adenocarcinoma. RNA sequencing identified a DEK::AFF2 fusion with breakpoints at DEK exon 7 and AFF2 exon 6, confirming the diagnosis. The tumor demonstrated positive PD-L1 expression with a combined positive score (CPS) of 40 and a low tumor mutational burden (TMB) of 0.5 mutations/Mb. This case highlights the diagnostic challenges posed by DEK::AFF2 fusion-associated carcinoma, underscores the importance of molecular profiling for accurate classification, and demonstrates the aggressive clinical behavior of this rare entity.

Journal Article↗

PubMed2026

A three-gene radioresistance signature predicts tumor progression in cervical cancer.

BACKGROUND: As a primary curative treatment for locally advanced cervical cancer, radiotherapy is frequently undermined by radioresistant tumor cells that evade cell death and subsequently drive post-treatment tumor progression. This study aimed to identify candidate genes associated with radioresistance in cervical cancer and to explore their potential in predicting unfavorable outcomes among radioresistant patients, thereby providing a reference for future research. METHODS: We screened for co-expressed genes using transcriptomic data from radiation non-complete response (NCR) cervical cancer patients in Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. Cox regression analyses were conducted to identify the most significant radioresistance-associated genes for constructing a prognostic model. The predictive performance of this model was further validated through logistic regression, weighted gene co-expression network analysis (WGCNA), and pan-cancer analyses. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was performed to quantify the expression levels of key genes in cervical cancer tissue samples from radiosensitive and radioresistant patients. RESULTS: The resulting prognostic model comprised three genes: MTMR11, VANGL1, and CD46. This gene panel was significantly associated with the prognosis of cervical cancer patients receiving radiotherapy and showed acceptable predictive performance across multiple cancer types. qRT-PCR analysis revealed that the expression patterns of MTMR11 and VANGL1 were generally consistent with radioresistance of cervical cancer, whereas CD46 exhibited an unexpected expression trend. CONCLUSIONS: Our findings indicate that MTMR11, VANGL1, and CD46 are associated with radioresistance and prognosis in cervical cancer. Their potential clinical utility, especially in predicting radiotherapy response at the individual patient level, requires further validation in larger, independent, and prospective cohorts.

Cervical cancer↗

PubMed2026

Genome-wide identification and expression profiling of HSD3B and SDR42E1 genes in the Pacific oyster (Crassostrea gigas): potential associations with gonadal development.

Sex steroids are lipid-soluble signaling molecules that regulate sex differentiation, reproductive development and physiological homeostasis in animals. 3β-Hydroxysteroid dehydrogenase/Δ5-Δ4 isomerase (3β-HSD) is a key steroidogenic enzyme, whereas SDR42E1, an extended short-chain dehydrogenase/reductase, has been implicated in sterol- and steroid-related metabolism. However, the composition, evolutionary relationships and expression patterns of the HSD3B- and SDR42E1-related genes in bivalve gonadal development remain poorly characterized. In this study, five PF01073-containing genes, comprising three CgHsd3b and two CgSdr42e1 genes, were identified in the Pacific oyster Crassostrea gigas. Phylogenetic analysis separated the proteins into HSD3B-related and SDR42E1-related groups, and gene-structure and motif analyses indicated subfamily-level divergence. All five proteins retained the SDR domain but differed in exon-intron structure and motif composition. Each contained the extended-SDR TGxxGxxG motif, whereas exact classical [ST]GxxxGxG and NNAG motifs were absent. Tyr- and Lys-equivalent residues were conserved, while the HSD3B1 Ser-equivalent position contained Thr in two C. gigas proteins and Ser in one. These features support their classification as extended-SDR proteins but do not establish enzymatic activity or substrate specificity. The three CgHsd3b genes were dispersed on one chromosome, whereas CgSdr42e1-1 and CgSdr42e1-2 were adjacent on another chromosome, suggesting a possible local duplication event for the CgSdr42e1 pair. Public RNA-seq data showed distinct tissue- and gonadal-stage expression patterns, with several genes displaying gonad-biased or female-stage-associated expression. Independent RT-qPCR profiling of the representative genes CgHsd3b-3 and CgSdr42e1-1 detected stage-dependent expression, although tissue rankings differed from those in the public RNA-seq datasets. These differences may reflect the use of independent biological samples, tissue composition, normalization procedures, and platform-specific measurements. Because enzymatic assays, metabolite measurements, cellular localization, and functional perturbation were not performed, the results identify candidate genes whose expression is associated with gonadal development rather than demonstrating regulatory roles. This study provides a comparative framework for future functional investigation of sterol- and steroid-related metabolism in bivalves.

Animals↗

PubMed2026

Genomic identification and functional characterization of the nuclear receptor gene family in relation to sex determination and gonad development in the Pacific oyster (Crassostrea gigas).

Nuclear receptors (NRs) are a large superfamily of transcription factors that control a wide range of physiological processes by modulating the expression of downstream target genes. Numerous studies have confirmed that NR family members play critical and conserved roles in sex determination and gonadal development across metazoans. However, in mollusks, systematic characterization of NRs and their potential functions in gonadal regulation remain largely unexplored. In this study, 46 NR gene family members in the Pacific oyster (Crassostrea gigas) were identified and assigned to eight subfamilies. All NR family members contain at least one of the two core domains (DNA-binding domain, DBD; ligand-binding domain, LBD), and conserved exon-intron structures were observed within the same subgroup, indicating their evolutionary conservation. Furthermore, expression profiling revealed high expression of CgNR2F, CgNR5A1-1, and CgNR0B1 in undifferentiated gonads, suggesting their potential involvement in sex determination. CgNR1A and CgNR2E5 were specifically expressed in female gonads and exhibited female-biased expression patterns, indicating a putative role in ovarian development. Moreover, CgNR3A and CgNR3B showed high expression levels during the undifferentiated stage and early male development stage, implying their possible participation in male gonadal development and gametogenesis. These results expand the understanding of the NR gene family in C. gigas and help elucidate the potential functions of NR genes in sex determination and gonadal development.

Animals↗

PubMed2026

LLPS-based classification and a novel prognostic signature reveal NRF1 as a therapeutic target in pancreatic cancer.

BACKGROUND: Aberrant liquid-liquid phase separation (LLPS) can alter biomolecular condensate functions and may influence pancreatic tumorigenesis and progression, but the specific role of LLPS regulators in prognosis and the tumor immune microenvironment (TIME) in pancreatic ductal adenocarcinoma (PDAC) remains unclear. METHODS: We integrated transcriptome data of LLPS regulator-related differentially expressed genes (DEGs; n = 298) in a cohort of 176 PDAC patients from TCGA. Three LLPS regulator subtypes (LS1-LS3) were identified through multi-omics analyses, and a prognostic LLPS subtype-related risk model (LRRPC) was developed and validated. Chromatin immunoprecipitation confirmed NRF1 binding to promoters of key risk genes, and in vitro and in vivo experiments assessed the effects of NRF1 targeting on tumor growth. RESULTS: The three LLPS regulator subtypes exhibited significant differences in prognosis, clinical features, genomic alterations, TIME patterns and predicted immunotherapy response. The LRRPC signature predicted prognosis and immunotherapy efficacy across cohorts and was associated with tumor biomarkers and immune infiltration. Nuclear Respiratory Factor 1 (NRF1) directly regulated hub genes such as FAM83A, RHOV and ITGB6, promoting PDAC cell proliferation, while its inhibition induced apoptosis and reduced tumor growth. CONCLUSIONS: This study proposes an LLPS-based stratification framework for PDAC, and the LRRPC model provides an LLPS subtype-related risk score that may assist personalized prognostic assessment and immunotherapy stratification. NRF1 emerges as a promising therapeutic candidate whose targeting can inhibit tumor progression in PDAC experimental models and warrants further evaluation.

Immunotherapy↗

PubMed2025

Beta-catenin/sirtuin 1/farnesoid X receptor pathway promotion of portal vein ligation and parenchymal transection-induced rapid liver regeneration.

BACKGROUND: By accelerating the regeneration of the future liver remnant, portal vein ligation and parenchymal transection allows for more extensive hepatectomy. Given that the mechanism remains poorly understood, the aim of this study was to investigate the mechanism of portal vein ligation and parenchymal transection-induced liver regeneration. METHODS: A portal vein ligation and parenchymal transection-induced liver regeneration mouse model was established, followed by RNA microarray analysis to identify candidate molecules. Genomic deletion and chemical manipulation of target molecules were used to explore their functions in portal vein ligation and parenchymal transection-induced liver regeneration. Validation was conducted using a diseased liver model and human samples. RESULTS: Portal vein ligation and parenchymal transection-induced liver regeneration was significantly accelerated compared with that in sham-operated mice (P < .05). An RNA microarray revealed that Sirtuin 1 is a crucial molecule in the proliferation of the future liver remnant. Regardless of whether Sirtuin 1 is inhibited chemically or through genetic deletion, portal vein ligation and parenchymal transection-induced liver regeneration is distinctly attenuated. Further investigation revealed that Sirtuin 1 promoted portal vein ligation and parenchymal transection-induced liver regeneration via the farnesoid X receptor. In addition, beta-catenin also was found to participate in the process of future liver remnant proliferation. Chemical inhibition of beta-catenin markedly impaired but activation of WNT/beta-catenin mildly enhanced portal vein ligation and parenchymal transection-induced liver regeneration (P < .05). Deletion of Sirtuin 1 blocked the facilitating effect of beta-catenin on portal vein ligation and parenchymal transection-induced liver regeneration. These findings were validated in diseased liver models and patient samples, confirming the correlation between the beta-catenin/Sirtuin 1/farnesoid X receptor pathway and portal vein ligation and parenchymal transection-induced liver regeneration. CONCLUSION: Activation of the beta-catenin/Sirtuin 1/farnesoid X receptor pathway offers critical mechanistic insights into accelerating portal vein ligation and parenchymal transection-induced liver regeneration. Modulation of beta-catenin/Sirtuin 1/farnesoid X receptor may therefore improve clinical outcomes in patients receiving staged hepatectomy.

Liver Regeneration↗