PubMed Health⌕ Search

Biomedical subjects

Ying Zhu

Publications and source records attributed to Ying Zhu.

At least 19 recordsLinked to original sources

A phase I clinical study of the safety, tolerability, pharmacokinetics and pharmacodynamics of SHR-2106, an anti-CD40 antibody, following single intravenous or subcutaneous administration in healthy participants.

BACKGROUND: SHR-2106 is a humanized IgG1 monoclonal antibody that blocks CD40-CD40L interactions and has demonstrated immunosuppressive activity and graft-prolonging effects in preclinical studies. This first-in-human Phase I study evaluated the safety, pharmacokinetics, pharmacodynamics, and immunogenicity of single intravenous or subcutaneous doses of SHR-2106 in healthy adults. METHODS: This randomized, double-blind, placebo-controlled Phase I study enrolled healthy participants. Fifty-one participants were enrolled in seven cohorts and received five intravenous doses (50-1200 mg) or two subcutaneous doses (300 and 600 mg). Safety, serum pharmacokinetics, CD40 occupancy on B cells, and anti-drug antibodies were assessed using standard clinical and bioanalytical methods. RESULTS: SHR-2106 demonstrated a favorable safety and tolerability profile, and most treatment-emergent adverse events were mild to moderate laboratory abnormalities with incidence rates comparable to placebo. SHR-2106 exhibited nonlinear pharmacokinetics consistent with target-mediated drug disposition, with a dose-dependent increase in geometric mean terminal half-life following intravenous administration (1.83-10.7 days). Absolute bioavailability after subcutaneous administration was approximately 60%. CD40 occupancy exceeded 80% within 24 h at all doses, with saturation duration increasing from 7 to 70 days across the intravenous dose range and remaining comparable between routes at matched doses. Anti-drug antibody incidence decreased with increasing intravenous dose and did not significantly affect pharmacokinetics or pharmacodynamics. CONCLUSION: SHR-2106 was well tolerated and achieved rapid and sustained CD40 engagement, supporting dose and route selection for Phase II studies.

Humans↗

Intellectual disability, neuroregression and adult-onset progressive dystonia due to a DLG4 pathogenic variant.

We report a 34-year-old male with childhood developmental delay, severe intellectual disability in adulthood, episodes of agitation with a previous diagnosis of schizoaffective disorder and adult-onset cognitive regression who developed progressive generalised dystonia due to a de novo DLG4 pathogenic loss-of-function variant. This case expands the phenotypic spectrum of recognised movement disorder manifestations associated with DLG4-related synaptopathy.

Humans↗

Genome-wide interactions with cadmium exposure in dysglycemia: Populational effects and molecular insights.

Dysglycemia is a complex metabolic disorder governed by the interplay between environmental exposures and genetic factors, yet the precise molecular mechanisms driving these gene-environment (G×E) interactions remains poorly understood. Here, we characterized the population-level landscape and molecular causality underlying the interactions between cadmium (Cd), a widespread environmental toxicant, and genetic susceptibility loci in dysglycemia. By conducting a Genome-wide Environmental Interaction (GWEI) study within a sub-cohort of the China National Human Biomonitoring (CNHBM) cohort (N = 1298), we identified 29 genetic risk loci that significantly interact with Cd burden to exacerbate elevated fasting plasma glucose levels. Functional enrichment integrated with metabolomic profiling unmasked a profound multi-omics convergence, positioning epigenetic modifications (e.g. H3K27me3) and zinc-finger transcription factors (e.g. OVOL2, KLFs) as central regulatory hubs that disrupt metabolic homeostasis. To establish causality, we demonstrated that the rs11743277 A>T variant at the lead G×E locus functions as a Cd-responsive enhancer element, facilitating recruitment of TEAD3 and upregulating TICAM2 expression in CRISPR/Cas9-edited HepG2 cells, especially upon Cd exposure. This initiates a TICAM2-mediated inflammatory response, with elevated pro-inflammatory cytokines (IFN-β, TNF-α, IL-6) impairing downstream insulin signaling and glucose utilization. Collectively, these findings establish a robust paradigm for G×E interactions in complex metabolic disorders, revealing how environmental stressors reprogram genetic susceptibilities through molecular checkpoints and paving the way for tailored, precision-prevention strategies in environmental health.

CRISPR/Cas9 editing↗

Molecular epidemiology of levofloxacin-resistant Klebsiella pneumoniae and the association of plasmid-mediated quinolone resistance genes with key biological phenotypes.

UNLABELLED: Klebsiella pneumoniae is a major opportunistic pathogen in China, yet the molecular epidemiology of quinolone resistance remains poorly characterized. This study analyzed 2,433 clinical isolates from 37 Chinese hospitals (2018-2022). The overall levofloxacin-non-susceptible (NS) rate was 53.60%, with urinary tract isolates showing higher resistance. Whole-genome sequencing identified 12 plasmid-mediated quinolone resistance (PMQR) genes. Among 1,304 NS strains, 74.54% carried at least one PMQR gene (mainly qnrS, qnrB, and aac(6')-Ib-cr), and 60.20% also had quinolone resistance-determining region (QRDR) mutations. Functional studies revealed diverse phenotypic impacts. Most PMQR genes conferred low-level resistance (minimum inhibitory concentration [MIC] = 1 mg/L), while qnrB52 and qnrB91 caused high-level resistance (MIC = 8-16 mg/L). Notably, qnrB91 reduced biofilm formation, indicating a trade-off between resistance and colonization. Growth assays showed that qnrB52, qnrB91, and qnrS1 inhibited normal growth, whereas qepA1 and qnrS1 enhanced growth under ethanol stress. Most PMQR genes (except qnrB6) attenuated bacterial adhesion. qepA1 promoted intracellular survival in macrophages, suggesting a role in chronic infection. Animal models confirmed that qnrB6, qnrB7, qnrVC6, and aac(6')-Ib-cr significantly enhanced virulence. This study is the first in China to report qnrVC6 and novel gyrA mutations (Ser83Ala/Val, Asp87Phe/His) in K. pneumoniae. It systematically reveals how PMQR genes influence infection by modulating resistance, immune evasion, and pathogenicity. These findings highlight that PMQR genes contribute not only to antibiotic resistance but also to virulence, suggesting that treatment strategies should consider specific PMQR genotypes. This research provides the largest-scale molecular epidemiological data and a theoretical basis for controlling quinolone-resistant K. pneumoniae in China. IMPORTANCE: Quinolone-resistant Klebsiella pneumoniae poses a serious threat to public health, yet the role of plasmid-mediated quinolone resistance (PMQR) genes beyond antibiotic resistance remains underexplored. In this largest-scale multicenter study in China, we analyzed 2,433 clinical isolates and discovered that PMQR genes do more than just confer drug resistance-they also influence bacterial growth, stress survival, biofilm formation, and the ability to evade or persist within host immune cells. Some PMQR genes even enhance virulence in an animal model. These findings challenge the traditional view of resistance genes as mere contributors to drug failure, revealing that they can also shape infection outcomes by altering bacterial behavior. Understanding these dual roles may guide more precise treatment strategies targeting specific PMQR genotypes.

Klebsiella pneumoniae↗

High-throughput single-cell proteomics and transcriptomics from same cells with a nanoliter-scale, spin-transfer approach.

Single-cell multiomic platforms provide a comprehensive snapshot of cellular states and cell types by offering critical insights into the spatiotemporal regulation of biomolecular networks at a systems level, thereby defining the basis of multicellularity. Here, we introduce nanoSPINS, an advanced platform that enables high-throughput profiling and integrative analysis of the transcriptome and proteome from the same single cells using RNA sequencing and isobaric labeling LC-MS-based proteomics, respectively. NanoSPINS can efficiently transfer mRNA-containing droplets across two microarrays via a centrifugation-based approach, while proteins are retained on the initial platform. Benchmarking of nanoSPINS on two cell lines demonstrates its ability to generate global proteomic and transcriptomic profiles that align well with previously established methodologies/platforms. The incorporation of isobaric TMTpro labeling into this single-cell multiomics platform significantly enhances the throughput of single-cell proteomic analyses. Through the high-throughput quantification of the proteome and transcriptome, nanoSPINS not only facilitates the identification of molecular features at both mRNA and protein level but also provides larger sample sizes for improved statistical power in clustering and differential abundance. Given the broad applicability of single-cell multiomics in biological research and clinical settings, we believe nanoSPINS represents a powerful platform for the characterization of heterogeneous cell populations.

Single-Cell Analysis↗

Plasma Proteomic Profiles Predict Individual Future Osteoarthritis Risk.

OBJECTIVE: Osteoarthritis (OA) is a widespread degenerative joint disease that causes a considerable socioeconomic burden. Despite progress in genetic and environmental insights, early diagnosis is still limited by the lack of evident symptoms during the initial phases and accurate biomarkers. This study aims to identify plasma proteins associated with future risk of OA and develop a predictive model. METHODS: We conducted a large-scale proteomic analysis of 45,307 participants from the UK Biobank, excluding those with baseline OA. Plasma samples were assayed using the Olink Explore Proximity Extension Assay targeting 1,463 unique proteins. Clinical variables and OA outcomes were extracted and linked to electronic health records. A predictive model was constructed using the LightGBM machine learning method, and SHapley Additive exPlanations (SHAP) were applied to evaluate the importance of variables. RESULTS: We identified a panel of proteins significantly associated with the risk of developing OA. Notably, after adjusting for multiple confounders, collagen type IX alpha 1 chain (COL9A1) and cartilage acidic protein 1 (CRTAC1) were the most significant predictors of incident OA, with hazard ratios of 1.54 (95% confidence interval [CI] 1.48-1.61) and 1.65 (95% CI 1.54-1.78), respectively. SHAP analysis allowed a profound interpretation of the contribution of each protein and clinical variable to the model, revealing the multifactorial nature of OA risk prediction. The temporal trajectories of plasma proteins indicated that the levels of COL9A1 and CRTAC1 began to deviate from normal for more than a decade before OA onset, suggesting their potential use in early detection strategies. The predictive model, developed using the LightGBM algorithm, integrated proteins with clinical covariates and demonstrated an area under the curve (AUC) of 0.729 for 5-year OA prediction, 0.721 for 10-year prediction, and 0.723 for all incident OA. The predictive accuracy of the model was further enhanced for hip and knee OA, achieving AUCs of 0.820 and 0.803 for 5-year predictions. CONCLUSION: Our study identified the role of plasma proteomics in predicting future OA risk, which could contribute to preemptive measures. The innovative model, which integrates proteomic biomarkers with clinical data, offers a potential tool for risk assessment, potentially optimizing OA management strategies and enhancing prevention efforts.

Humans↗

Adaptation for Staphylococcus aureus to hosts via insertion mutation in the accessory gene regulator agrC gene: decreased virulence and enhanced persistence capacity.

UNLABELLED: Staphylococcus aureus is an important human pathogen due to its vast array of virulence factors regulated by multiple regulatory mechanisms, including the accessory gene regulator. In this study, two S. aureus strains were simultaneously isolated from the blood of a febrile patient, belonging to the same clone, designated as 23H with a complete hemolytic phenotype, and 23B, exhibiting an incomplete hemolytic phenotype. The genomic comparison between strains 23B and 23H revealed that 23B had a single adenine base insertion at position 923 in the agrC gene, leading to a functional loss of the encoded AgrC. Experimental findings showed that strain 23B had decreased hemolytic activity, lower cytotoxicity against human alveolar epithelial A549 cells and in the Galleria mellonella model, and a reduced ability to survive intracellularly after infecting macrophages, in comparison to 23H. Conversely, 23B exhibited enhanced biofilm formation, greater adherence to A549 cells, and increased persistence in the face of vancomycin and daptomycin treatment. Transcriptomic analysis revealed that 23B upregulated surface protein-encoding genes while simultaneously reducing the expression levels of virulence factors, highlighting the intricate regulatory adjustments facilitating its persistence and reducing pathogenic potential. ATP assay results indicated that 23B maintained elevated ATP levels during the exponential phase yet exhibited reduced levels in the stationary phase when compared with 23H. Our findings suggested that the mutation in the agrC gene of S. aureus results in diminished virulence but markedly enhances persistence. This mutated strain warrants clinical attention because it may lead to treatment failures and persist in patients. IMPORTANCE: In clinical antimicrobial therapy, bacterial strains often develop resistance to antimicrobial agents. Additionally, mutations in their gene regulatory networks can increase their persistence, especially in immunocompromised patients. This study identified an insertion mutation in the accessory gene regulator, agrC gene, carried by a Staphylococcus aureus strain isolated from the blood of a febrile patient, leading to the functional loss of AgrC. Further research revealed that despite the reduced virulence of the mutated strain, it significantly bolstered the capacity to adapt and endure within the host during prolonged infections. This was evidenced by increased adhesion and biofilm formation capabilities, development of antimicrobial tolerance, and decreased ATP levels linked to persistence. Therefore, monitoring these mutations in S. aureus is crucial clinically, as they can complicate treatment strategies.

Staphylococcus aureus↗

Proteome-Scale Tissue Mapping Using Mass Spectrometry Based on Label-Free and Multiplexed Workflows.

Multiplexed bimolecular profiling of tissue microenvironment, or spatial omics, can provide deep insight into cellular compositions and interactions in healthy and diseased tissues. Proteome-scale tissue mapping, which aims to unbiasedly visualize all the proteins in a whole tissue section or region of interest, has attracted significant interest because it holds great potential to directly reveal diagnostic biomarkers and therapeutic targets. While many approaches are available, however, proteome mapping still exhibits significant technical challenges in both protein coverage and analytical throughput. Since many of these existing challenges are associated with mass spectrometry-based protein identification and quantification, we performed a detailed benchmarking study of three protein quantification methods for spatial proteome mapping, including label-free, TMT-MS2, and TMT-MS3. Our study indicates label-free method provided the deepest coverages of ∼3500 proteins at a spatial resolution of 50 μm and the highest quantification dynamic range, while TMT-MS2 method holds great benefit in mapping throughput at >125 pixels per day. The evaluation also indicates both label-free and TMT-MS2 provides robust protein quantifications in identifying differentially abundant proteins and spatially covariable clusters. In the study of pancreatic islet microenvironment, we demonstrated deep proteome mapping not only enables the identification of protein markers specific to different cell types, but more importantly, it also reveals unknown or hidden protein patterns by spatial coexpression analysis.

Proteome↗

Proteome-scale tissue mapping using mass spectrometry based on label-free and multiplexed workflows.

Multiplexed bimolecular profiling of tissue microenvironment, or spatial omics, can provide deep insight into cellular compositions and interactions in healthy and diseased tissues. Proteome-scale tissue mapping, which aims to unbiasedly visualize all the proteins in a whole tissue section or region of interest, has attracted significant interest because it holds great potential to directly reveal diagnostic biomarkers and therapeutic targets. While many approaches are available, however, proteome mapping still exhibits significant technical challenges in both protein coverage and analytical throughput. Since many of these existing challenges are associated with mass spectrometry-based protein identification and quantification, we performed a detailed benchmarking study of three protein quantification methods for spatial proteome mapping, including label-free, TMT-MS2, and TMT-MS3. Our study indicates label-free method provided the deepest coverages of ~3500 proteins at a spatial resolution of 50 µm and the highest quantification dynamic range, while TMT-MS2 method holds great benefit in mapping throughput at >125 pixels per day. The evaluation also indicates both label-free and TMT-MS2 provide robust protein quantifications in identifying differentially abundant proteins and spatially co-variable clusters. In the study of pancreatic islet microenvironment, we demonstrated deep proteome mapping not only enables the identification of protein markers specific to different cell types, but more importantly, it also reveals unknown or hidden protein patterns by spatial co-expression analysis.

Journal Article↗

Protein-free fed-batch culture of non-GS NS0 cell lines for production of recombinant antibodies.

Presented is a novel antibody production platform based on the fed-batch culture of recombinant, NS0-derived cell lines. A standardized fed-batch cell culture process was developed for five non-GS NS0 cell lines using enriched and optimized protein-free, cholesterol-free, and chemically defined basal and feed media. The process performed reproducibly and scaled faithfully from the 2-L to the 100-L bioreactor scale achieving a volumetric productivity of > 120 mg/L per day. Fed-batch cultures for all five cell lines exhibited significant lactate consumption when the cells entered the stationary or death phase. Peak and final lactate concentrations were low relative to a previously developed fed-batch process (FBP). Such low lactate production and high lactate consumption rates were unanticipated considering the fed-batch culture basal medium has an unconventionally high initial glucose concentration of 15 g/L, and an overall glucose consumption in excess of 17 g/L. The potential of this process platform was further demonstrated through additional media optimization, which has resulted in a final antibody concentration of 2.64 +/- 0.19 g/L and volumetric productivity of > 200 mg/L per day in a 13-day FBP for one of the five production cell lines. Use of this standardized protein-free, cholesterol-free NS0 FBP platform enables consistency in development time and cost effectiveness for manufacturing of therapeutic antibodies.

Animals↗

Simultaneously inhibition of HIV and HBV replication through a dual small interfering RNA expression system.

Human immunodeficiency virus (HIV) is often acquired in individuals already infected with hepatitis B virus (HBV) as a result of shared routes of transmission. Since current options for the treatment of HIV and HBV infections are limited, there is an essential need for the development of effective therapies against HIV/HBV co-infections. RNA interference (RNAi) has been used as a powerful tool to silence genes in cells and animals. In this study, we developed a small interfering RNA generation system that expressed two different siRNAs to target the HBs gene of HBV and the gp120 gene of HIV in Bel-7402 and HEK293T cells, respectively. Our results demonstrated that the two siRNA molecules could simultaneously inhibit the expression of HBs and gp120 by 81% and 89%, respectively. In addition, dual siRNA molecules significantly decreased the production of HBs, and simultaneously inhibited the replication of HBV and HIV. This dual siRNA generation system not only proved to be a novel approach for studying functions of multiple genes simultaneously, but also provides a potential approach for the treatment and prevention of HIV and HBV co-infection.

Animals↗

Inhibition of SARS-CoV gene expression by adenovirus-delivered small hairpin RNA.

OBJECTIVE: Severe acute respiratory syndrome (SARS) is a highly contagious and lethal disease caused by a new type of coronavirus, SARS-associated coronavirus (SARS-CoV). Currently, there is no efficient treatment and prevention for this disease. We constructed recombinant adenoviral vectors that can express shRNAs, which inhibited the expression of SARS-CoV genes effectively in mammalian cells. METHODS: In this study, we designed several plasmids that express small hairpin RNA molecules (shRNA) specifically targeting to the genes encoding for the SARS-CoV nucleocapsid (N) protein and envelope (E) protein, respectively. Effective shRNA molecules to the viral genes were screened and identified, and then constructed into adenovirus vectors. The effects of adenovirus-delivered small hairpin RNA on SARS-CoV gene expression were determined by RT-PCR, Western blot, and luciferase activity assays. RESULTS: The levels of viral mRNAs and viral proteins of the targets were significantly decreased or completely inhibited in cell lines after being infected with the recombinant adenoviruses that expressed specific shRNA molecules. CONCLUSIONS: Since many cell types can be efficiently infected by adenovirus, recombinant adenoviruses could serve as an alternative powerful tool for shRNA delivery and for gene suppression, especially when the targeted cells are resistant to transfection by DNA or RNA. With availability of high titers of adenoviruses and uniform and rapid infection, this approach would have foreseeable wide applications both in experimental biology and molecular medicine.

Adenoviridae↗

Neural basis of cultural influence on self-representation.

Culture affects the psychological structure of self and results in two distinct types of self-representation (Western independent self and East Asian interdependent self). However, the neural basis of culture-self interaction remains unknown. We used fMRI to measured brain activity from Western and Chinese subjects who judged personal trait adjectives regarding self, mother or a public person. We found that the medial prefrontal cortex (MPFC) and anterior cingulate cortex (ACC) showed stronger activation in self- than other-judgment conditions for both Chinese and Western subjects. However, relative to other-judgments, mother-judgments activated MPFC in Chinese but not in Western subjects. Our findings suggest that Chinese individuals use MPFC to represent both the self and the mother whereas Westerners use MPFC to represent exclusively the self, providing neuroimaging evidence that culture shapes the functional anatomy of self-representation.

Adult↗

A quantitative comet assay: imaging and analysis of virus plaques formed with a liquid overlay.

Although the plaque assay defines a "gold-standard" for measuring virus infectivity, its reliance on plaque counting limits its sensitivity. When the assay is performed with a liquid overlay, instead of agar overlay, spontaneous flows can promote a uni-directional spread of infection, creating elongated regions of cytopathology that resemble comets. As a model system comet and plaque cultures of vesicular stomatitis virus (VSV) on baby hamster kidney (BHK-21) cells were compared. Host-cell monolayers were infected with VSV particles, incubated 15 h in the presence of liquid or agar overlays and stained. VSV formed significantly larger comets than plaques, consistent with a mechanism of flow-enhanced spread. When antiviral drug (5-fluorouracil) was incorporated into the liquid overlay, comet sizes were reduced in a dose-dependent manner. Images of infected monolayers, acquired using a simple digital scanner, enabled a quantification of the inhibitory effect of the drug on infectivity. The resulting measure of drug susceptibility was found to be 18-fold more sensitive than the IC(50) measure attained by the traditional plaque-reduction assay. This quantitative comet assay has the potential to similarly enhance the sensitivity of infection measures for other plaque-forming viruses.

Animals↗

Obligate multivalent recognition of cell surface tomoregulin following selection from a multivalent phage antibody library.

A therapeutic antibody candidate (AT-19) isolated using multivalent phage display binds native tomoregulin (TR) as a mul-timer not as a monomer. This report raises the importance of screening and selecting phage antibodies on native antigen and reemphasizes the possibility that potentially valuable antibodies are discarded when a monomeric phage display system is used for screening. A detailed live cell panning selection and screening method to isolate multivalently active antibodies is described. AT-19 is a fully human antibody recognizing the cell surface protein TR, a proposed prostate cancer target for therapeutic antibody internalization. AT-19 was isolated from a multivalent single-chain variable fragment (scFv) antibody library rescued with hyperphage. The required multivalency for isolation of AT-19 is supported by fluorescence activated cell sorting data demonstrating binding of the multivalent AT-19 phage particles at high phage concentrations and failure of monovalent particles to bind. Pure monomeric scFv AT-19 does not bind native receptor on cells, whereas dimeric scFv or immunoglobulin G binds with nanomolar affinity. The isolation of AT-19 antibody with obligate bivalent binding activity to native TR is attributed to the use of a multivalent display of scFv on phage and the method for selecting and screening by alternate use of 2 recombinant cell lines.

Animals↗

A method for determining pyrene in mucus using synchronous fluorimetry with multiple standard additions.

A new method was proposed to determine pyrene in mucus, which combined the synchronous fluorimetry with the multiple standard addition method (SFMSA). The method was used to determine pyrene in mucus directly without pretreatment. The method detection limit (MDL) for pyrene in mucus was measured as 0.47 ng/ml with a relative standard deviation of 12.7% (n = 7). The standard addition graph was linear in the range 0.05-50.00 ng/ml (r(2) = 0.9989). SFMSA was validated using a GC/MS method as a reference method, and nice agreement was found. The pyrene in mucus can be directly monitored by SFMSA without solvent extraction of samples. This indicates that SFMSA is more timesaving, less laborious and cheaper than the GC/MS method with solvent extraction. SFMSA has lower MDL and higher average recovery than the GC/MS method.

Animals↗

Immunoactive polysaccharide-rich fractions from Panax notoginseng.

Panax notoginseng is a commonly used medicinal plant in south-western China. In a previous study, a sequential solubilisation of P. notoginseng high-molecular-weight (HMW) polymers using phenol-acetic acid-water, hot water, weak and strong alkali was performed to determine the structure of the component polysaccharides and proteins. The effects of these extracted HMW fractions on the human complement system, polymorphonuclear neutrophils (PMN) and peripheral blood mononuclear cells (PBMC) are reported here. Fr (1MKOH), which was extracted with 1 M KOH, showed the strongest complement-fixing activity and priming of reactive oxygen species (ROS) production by PMNs, as well as a mitogenic effect. Fr (1MKOH) was further fractionated by anion-exchange chromatography followed by gel-permeation chromatography. 1MD3-G2, the fraction most strongly bound to the DEAE anion-exchange column with a molecular weight of 1140 kDa, showed the highest complement-fixing activity. It is composed of acidic polysaccharides [including glucuronoarabinoxylan (GAX), homogalacturonan (HGA), rhamnogalacturonan I (RG I)], neutral polysaccharides (4-galactan and arabinan), and some protein.

Cells, Cultured↗

Inhibition of survivin reduces cell proliferation and induces apoptosis in human endometrial cancer.

BACKGROUND: Endometrial cancer is a common gynecologic malignancy among women. The molecular mechanisms involved in the progression of endometrial cancer are unclear, which has hampered the development of an effective treatment. Survivin, a newly identified member of the inhibitor of apoptosis (IAP) family, regulates 2 critical processes in neoplastic transformation: cell proliferation and apoptosis. METHODS: Survivin mRNA and protein expression levels were analyzed in human normal cycling endometrium, atypical endometrium, and endometrial adenocarcinoma by immunohistochemical, reverse-transcriptase polymerase chain reaction (RT-PCR), and Western blot analyses. To study the biological function of survivin in endometrial cancer, RNA interference was applied to knock down survivin expression in the Ishikawa endometrial cancer cell line by recombinant plasmids producing survivin small hairpin RNA. Furthermore, the signal pathway that regulates survivin expression was investigated. RESULTS: Higher levels of survivin mRNA and protein expression were observed in endometrial adenocarcinomas than in atypical or normal endometrium. Immunohistochemical staining revealed that 83.3% (50 of 60) of endometrial adenocarcinoma samples, 55.0% (11 of 20) of atypical endometrium samples, and 25.0% (5 of 20) of normal endometrium samples were positive for survivin protein. Inhibition of survivin by RNA interference reduced cell proliferation and induced apoptosis in Ishikawa cells by down-regulating cyclin D1 and phosphorylated RB and activating caspase-3 and caspase-8. The authors also found that the MAPK pathway was a signal transduction pathway upstream of survivin. Epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha) upregulated survivin protein expression by activating the MAPK pathway in endometrial cancer cells. CONCLUSIONS: Survivin is an attractive target for endometrial cancer treatment. Growth factors could regulate survivin expression by activating the MAPK pathway.

Adenocarcinoma↗