A GAN-based anomaly detector using multi-feature fusion and selection.

In numerous applications, abnormal samples are hard to collect, limiting the use of well-established supervised learning methods. GAN-based models which trained in an unsupervised and single feature set manner have been proposed by simultaneously considering the reconstruction error and the latent space deviation between normal samples and abnormal samples. However, the ability to capture the input distribution of each feature set is limited. Hence, we propose an unsupervised and multi-feature model, Wave-GANomaly, trained only on normal samples to learn the distribution of these normal samples. The model predicts whether a given sample is normal or not by its deviation from the distribution of normal samples. Wave-GANomaly fuses and selects from the wave-based features extracted by the WaveBlock module and the convolution-based features. The WaveBlock has proven to efficiently improve the performance on image classification, object detection, and segmentation tasks. As a result, Wave-GANomaly achieves the best average area under the curve (AUC) on the Canadian Institute for Advanced Research (CIFAR)-10 dataset (94.3%) and on the Modified National Institute of Standards and Technology (MNIST) dataset (91.0%) when compared to existing state-of-the-art anomaly detectors such as GANomaly, Skip-GANomaly, and the skip-attention generative adversarial network (SAGAN). We further verify our method by the self-curated real-world dataset, the result show that our method is better than GANomaly which only use single feature set for training the model.

RACK1 promotes the occurrence and progression of cervical carcinoma.

BACKGROUND: RACK1 has been identified as a multifunctional cytosolic protein, and plays a pivotal role in multiple biological responses involved in several kinds of tumors, while its effect in cervical cancer has not been well elucidated yet. The study aimed to investigate the role of RACK1 in cervical cancer occurrence and progression. METHODS: The expression of RACK1 in cervical specimens was measured by immunohistochemical staining and Western blot assay. Transgenic mice were used to detect the role of RACK1 in modulating tumorigenesis in vivo. Cervical carcinoma cell lines were used to explore the underlying mechanisms of RACK1 on the behaviors of tumor cells in vitro. RESULTS: We found that RACK1 expression was upregulated in cancer tissues compared with adjacent tissues, and its expression was gradually increased from cervictis, and cervical intraepithelial neoplasis (CIN) to carcinoma. Genetic overexpression of RACK1 facilitated tumor formation and growth in nude mice. Mechanism studies disclosed that RACK1 over-expression prolonged the G0 /G1 phase by up-regulating the expression of cyclinD1, down-regulating p21 and p27 probably by modulating the phosphorylation of AKT. CONCLUSIONS: Taken together, we concluded that RACK1 stimulates tumorigenesis and progression of cervical cancer via modulating the proliferation of tumor cells, implying that targeting RACK1 may serve as a promising method for cervical cancer therapy.

Toward surface defect detection in electronics manufacturing by an accurate and lightweight YOLO-style object detector.

In electronics manufacturing, surface defect detection is very important for product quality control, and defective products can cause severe customer complaints. At the same time, in the manufacturing process, the cycle time of each product is usually very short. Furthermore, high-resolution input images from high-resolution industrial cameras are necessary to meet the requirements for high quality control standards. Hence, how to design an accurate object detector with real-time inference speed that can accept high-resolution input is an important task. In this work, an accurate YOLO-style object detector was designed, ATT-YOLO, which uses only one self-attention module, many-scale feature extraction and integration in the backbone and feature pyramid, and an improved auto-anchor design to address this problem. There are few datasets for surface detection in electronics manufacturing. Hence, we curated a dataset consisting of 14,478 laptop surface defects, on which ATT-YOLO achieved 92.8% mAP0.5 for the binary-class object detection task. We also further verified our design on the COCO benchmark dataset. Considering both computation costs and the performance of object detectors, ATT-YOLO outperforms several state-of-the-art and lightweight object detectors on the COCO dataset. It achieves a 44.9% mAP score and 21.8 GFLOPs, which is better than the compared models including YOLOv8-small (44.9%, 28.6G), YOLOv7-tiny-SiLU (38.7%, 13.8G), YOLOv6-small (43.1%, 44.2G), pp-YOLOE-small (42.7%, 17.4G), YOLOX-small (39.6%, 26.8G), and YOLOv5-small (36.7%, 17.2G). We hope that this work can serve as a useful reference for the utilization of attention-based networks in real-world situations.

Integrating the Z-scheme heterojunction and hot electrons injection into a plasmonic-based Zn2In2S5/W18O49 composite induced improved molecular oxygen activation for photocatalytic degradation and antibacterial performance.

The semiconductor-based photocatalysts with local surface plasmon resonance (LSPR) effect can extend light response to near-infrared region (NIR), as well as promote charge-carriers transfer, which provide a novel insight into designing light-driven photocatalyst with excellent photocatalytic performance. Here, we designed cost-effective wide-spectrum Zn2In2S5/W18O49 composite with enhanced photocatalytic performance based on a dual-channel charge transfer pathway. Benefiting from the synergistic effect of Z-scheme heterostructure and unique LSPR effect, the interfacial charge-carriers transfer rate and light-absorbing ability of Zn2In2S5/W18O49 were enhanced significantly under visible and NIR (vis-NIR) light irradiation. More reactive oxygen species (ROS) were formed by efficient molecular oxygen activation, which were the critical factors for both Escherichia coli (E. coli) photoinactivation and tetracycline (TC) photodegradation. The enhancement of molecular oxygen activation (MOA) ability was verified via quantitative analyses, which evaluated the amount of ROS through degrading nitrotetrazolium blue chloride (NBT) and p-phthalic acid (TA). By combining theoretical calculations with diverse experimental results, we proposed a credible photocatalytic reaction mechanism for antibiotic degradation and bacteria inactivation. This study develops a new insight into constructing promising photocatalysts with efficient photocatalytic activity in practical wastewater treatment.

Corrigendum: Foot-and-Mouth Disease Virus Capsid Protein VP1 Antagonizes TPL2-Mediated Activation of the IRF3/IFN-ß Signaling Pathway to Facilitate the Virus Replication.

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YY1-Induced lncRNA PART1 Enhanced Resistance of Ovarian Cancer Cells to Cisplatin by Regulating miR-512-3p/CHRAC1 Axis.

Chemoresistance is one of the major obstacles encountered in ovarian cancer (OC) therapy. Long noncoding RNA PART1 has been reported to be involved in the tumorigenesis of several types of cancers. However, the biological role of PART1 in the chemoresistance of OC is still unclear. In this study, it was found that the expression levels of PART1 and CHRAC1 were increased and miR-512-3p expression was decreased in cisplatin (DDP)-resistant OC cell lines. The depletion of PART1 enhanced the DDP sensitivity of DDP-resistant OC cells, as indicated by the inhibition of cell proliferation, migration, and invasion, and promotion of cell apoptosis. In the upstream mechanism exploration, we discovered that PART1 was induced by YY1 transcription factor. Moreover, it was identified that miR-512-3p was a target of PART1, and PART1 regulated the DDP resistance of OC through miR-512-3p. In addition, we screened the candidate genes of miR-512-3p., and confirmed that CHRAC1 was the downstream gene of miR-512-3p. Furthermore, the knockdown of CHRAC1 inhibited proliferation, migration, and invasion, and accelerated apoptosis of DDP-resistant OC cells, which was counteracted after the inhibition of miR-512-3p. Finally, we observed that PART1 regulated the expression of CHRAC1 through miR-512-3p. In conclusion, we demonstrated that YY1-induced PART1 accelerated DDP resistance of OC through miR-512-3p/CHRAC1 axis, suggesting PART1 may be a promising therapeutic target for DDP-resistant OC patients.

The PB1 protein of influenza A virus inhibits the innate immune response by targeting MAVS for NBR1-mediated selective autophagic degradation.

Influenza A virus (IAV) has evolved various strategies to counteract the innate immune response using different viral proteins. However, the mechanism is not fully elucidated. In this study, we identified the PB1 protein of H7N9 virus as a new negative regulator of virus- or poly(I:C)-stimulated IFN induction and specifically interacted with and destabilized MAVS. A subsequent study revealed that PB1 promoted E3 ligase RNF5 to catalyze K27-linked polyubiquitination of MAVS at Lys362 and Lys461. Moreover, we found that PB1 preferentially associated with a selective autophagic receptor neighbor of BRCA1 (NBR1) that recognizes ubiquitinated MAVS and delivers it to autophagosomes for degradation. The degradation cascade mediated by PB1 facilitates H7N9 virus infection by blocking the RIG-I-MAVS-mediated innate signaling pathway. Taken together, these data uncover a negative regulatory mechanism involving the PB1-RNF5-MAVS-NBR1 axis and provide insights into an evasion strategy employed by influenza virus that involves selective autophagy and innate signaling pathways.

Motion parameter estimation of multitonal sources with a single hydrophone.

In this letter, a method is proposed to estimate the motion parameters of a multitonal source with a single hydrophone when only the acquisition time of the pressure field is known. Source motion parameters, including the time of closest point of approach (tCPA) and the ratio of the range at the closest point of approach to the source speed ( rCPA/v) are obtained by correlation of two resampled tonal signals. Only two tones emitted by the same source and a value of the waveguide invariant are required. The proposed method is validated by simulation and data from the SWellEx-96 experiment.

The Nucleoprotein of H7N9 Influenza Virus Positively Regulates TRAF3-Mediated Innate Signaling and Attenuates Viral Virulence in Mice.

H7N9 influenza A virus (IAV) is an emerged contagious pathogen that may cause severe human infections, even death. Understanding the precise cross talk between virus and host is vital for the development of effective vaccines and therapeutics. In the present study, we identified the nucleoprotein (NP) of H7N9 IAV as a positive regulator of RIG-I like receptor (RLR)-mediated signaling. Based on a loss-of-function strategy, we replaced H1N1 (mouse-adapted PR8 strain) NP with H7N9 NP, by using reverse genetics, and found that the replication and pathogenicity of recombinant PR8-H7N9NP (rPR8-H7N9NP) were significantly attenuated in cells and mice. Biochemical and cellular analyses revealed that H7N9 NP specifically interacts with tumor necrosis factor receptor (TNFR)-associated factor 3 (TRAF3) after viral infection. Subsequently, we identified a PXXQXS motif in the H7N9 NP that may be a determinant for the NP and TRAF3 interaction. Furthermore, H7N9 NP stabilized TRAF3 expression via competitively binding to TRAF3 with cellular inhibitor of apoptosis 2 (cIAP2), leading to the inhibition of the Lys48-linked polyubiquitination and degradation of TRAF3. Taken together, these data uncover a novel mechanism by which the NP of H7N9 IAV positively regulates TRAF3-mediated type I interferon signaling. Our findings provide insights into virus and host survival strategies that involve a specific viral protein that modulates an appropriate immune response in hosts.IMPORTANCE The NS1, PB2, PA-X, and PB1-F2 proteins of influenza A virus (IAV) are known to employ various strategies to counteract and evade host defenses. However, the viral components responsible for the activation of innate immune signaling remain elusive. Here, we demonstrate for the first time that the NP of H7N9 IAV specifically associates with and stabilizes the important adaptor molecule TRAF3, which potentiates RLR-mediated type I interferon induction. Moreover, we reveal that this H7N9 NP protein prevents the interaction between TRAF3 and cIAP2 that mediates Lys48-linked polyubiquitination of TRAF3 for degradation. The current study revealed a novel mechanism by which H7N9 NP upregulates TRAF3-mediated type I interferon production, leading to attenuation of viral replication and pathogenicity in cells and mice. Our finding provides a possible explanation for virus and host commensalism via viral manipulation of the host immune system.

miR-211-5p is down-regulated and a prognostic marker in bladder cancer.

BACKGROUND: The micro RNA (miRNA)/histone deacetylase 9 (HDAC9) signaling axis has been reported to be involved in initiating and developing multiple malignant tumors. In the present study, we aimed to determine whether miR-211-5p serves as a post-transcriptional regulator in bladder cancer (BCa) cell proliferation and apoptosis by targeting HDAC9. METHODS: miRNA expression profiling of BCa tissues and para-carcinoma tissues was screened by miRNA microarray. After transfection with miR-211-5p mimics or short hairpin RNA of HDAC9 (sh-HDAC9), mRNA and protein expression was evaluated using a quantitative reverse transcription-polymerase chain reaction and western blotting, respectively. A bioinformatics algorithm was used, and a dual-luciferase reporter assay was performed to validate HDAC9 as a direct target of miR-211-5p. Cell proliferation was analyzed by the 3-(4, 5-dimethylthiazl2-yl)-2,5-diphenyltetazolium bromide (MTT) assay. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) detection was used to evaluate apoptosis in 5637 and T24 cells. A transwell assay was used to assess migration and invasion. RESULTS: miR-211-5p is down-regulated in BCa tumor tissues and cell lines. miR-211-5p is identified as an independent biomarker for predicting overall survival. HDAC9 is a direct target of miR-211-5p, and overexpression of miR-211-5p represses HDAC9 protein expression in vitro. Overexpression of miR-211-5p or HDAC9 knockdown significantly inhibits proliferation, migration and invasion of 5637 and T24 cells, and also induces cell apoptosis. CONCLUSIONS: miR-211-5p may play a role as a tumor suppressor and as a favourable prognostic marker in BCa.

Orf Virus VIR Antagonizes p53-Mediated Antiviral Effects to Facilitate Viral Replication.

As a zoonotic disease, ovine contagious pustular dermatitis (Orf) is a serious threat to sheep as well as humans. Orf virus (ORFV) interferon resistance protein (VIR) is the principal virulence protein that encodes a dsRNA-binding protein to inhibit host antiviral response. p53 is one of the key proteins of the host antiviral innate immunity. It not only enhances type I interferon secretion but also induces apoptosis in infected cells, and plays a crucial role in the immune response against various viral infections. However, it remains to be elucidated what role p53 plays in ORFV replication and whether ORFV's own protein VIR regulates p53 expression to promote self-replication. In this study, we showed that p53 has an antiviral effect on ORFV and can inhibit ORFV replication. In addition, ORFV nonstructural protein VIR interacts with p53 and degrades p53, which inhibits p53-mediated positive regulation of downstream antiviral genes. This study provides new insight into the immune evasion mediated by ORFV and identifies VIR as an antagonistic factor for ORFV to evade the antiviral response.

Foot-and-Mouth Disease Virus Capsid Protein VP1 Antagonizes TPL2-Mediated Activation of the IRF3/IFN-ß Signaling Pathway to Facilitate the Virus Replication.

Foot-and-mouth disease (FMD) is a severe, highly contagious viral disease of cloven-hoofed animals. In order to establish an infection, the FMD virus (FMDV) needs to counteract host antiviral responses. Tumor progression locus 2 (TPL2), a mitogen-activated protein kinase, can regulate innate and adaptive immunity; however, its exact mechanisms underlying TPL2-mediated regulation of the pathogenesis of FMDV infection remain unknown. In this study, we confirmed that TPL2 could inhibit FMDV replication in vitro and in vivo. The virus replication increased in Tpl2-deficient suckling mice in association with reduced expression of interferon-stimulated genes interferon-α (IFN-α) and myxovirus resistance (MX2) and significantly reduced expression of C-X-C motif chemokine ligand 10 (CXCL10), interferon regulatory factor 3 (IRF3), and IRF7, while the phosphorylation of IRF3 was not detected. Moreover, the interactions between TPL2 and VP1 were also confirmed. The overexpression of TPL2 promoted IRF3-mediated dose-dependent activation of the IFN-ß signaling pathway in association with interactions between IRF3 and TPL2. VP1 also inhibited phosphorylation of TPL2 at Thr290, while Thr290 resulted as the key functional site associated with the TPL2-mediated antiviral response. Taken together, this study indicated that FMDV capsid protein VP1 antagonizes TPL2-mediated activation of the IRF3/IFN-ß signaling pathway for immune escape and facilitated virus replication.

Systematic Profiling and Evaluation of Structure-based Kinase-Inhibitor Interactome in Cervical Cancer by Integrating In Silico Analyses and In Vitro Assays at Molecular and Cellular Levels.

Various protein kinases are implicated in the pathogenesis of human cervical cancer and many kinase inhibitors have been used to regulate the activity of protein kinases involved in the disease signaling networks. In the present study, a systematic kinase-inhibitor interactome is created for various small-molecule inhibitors across diverse cervical cancer-related kinases by using ontology enrichment, molecular docking, dynamics simulation and energetics analysis. The interactome profile is examined in detail with heatmap analysis and heuristic clustering to derive promising inhibitors that are highly potential to target the kinome of human cervical cancer in a multi-target manner. A number of hit and unhit inhibitors are selected and their cell-suppressing effects are tested against human cervical carcinoma HeLa, from which several inhibitor compounds with high cytotoxicity are successfully identified. A further kinase assay confirms that these inhibitors can generally target their noncognate kinases HER3 and BRaf in cervical cancer with a high or moderate activity; the activity profile are comparable with or even better than that of cognate kinases inhibitors, with IC50 values ranging between 4.8 and 340.6 nM for HER3 and between 37.2 and 638.2 nM for BRaf. This work would help to identify those unexpected kinase-inhibitor interactions in human cervical cancer and to develop new and efficient therapeutic strategy combating the disease.

Constructing magnetic and high-efficiency AgI/CuFe2O4 photocatalysts for inactivation of Escherichia coli and Staphylococcus aureus under visible light: Inactivation performance and mechanism analysis.

Magnetic materials usually exhibit advanced performance in many areas for their easy separating and recycle ability. In this study, silver iodide/copper ferrite (AgI/CuFe2O4) catalysts with excellent magnetic property were successfully synthesized and characterized by a series of techniques. Two typical bacteria Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) were applied to estimate the photocatalytic inactivation performance of obtained AgI/CuFe2O4 catalysts. Results revealed that the AgI/CuFe2O4 (12.5% AgI) composite could absolutely inactivate 3 × 109 CFU/mL E. coli and 2.7 × 108 CFU/mL S. aureus cells severally in 50 min and 40 min under visible light irradiation, which showed a much higher photo-disinfection activity than monomers. Transmission electron microscopy was used to study the biocidal action of this nanocatalyst, the results confirmed that the treated E. coli cells were damaged, the nanocatalyst permeated into cells and resulting in death of cells. Besides, it was found that the destruction of bacterial membrane together with substantial leaked potassium ion (K+) which caused by the photo-generated reactive species superoxide radical (O2-) and holes (h+) could be the direct disinfection principles. For a deep insight into practical applications, the influences of different catalyst concentrations and reaction pH were also taken into discussion in details. The overall results indicated the novel photocatalyst with strong redox capacity and outstanding reusability can be widely employed in bacteria elimination.

Advancement in TPL2-regulated innate immune response.

Tumor progression locus 2 (TPL2) is a serine/threonine kinase that belongs to the MAP3K family. The activated TPL2 regulates the innate immune-relevant signaling pathways, such as ERK, JNK, and NF-κB, and the differentiation of immune cells, for example, CD4+ T and NK cells. Therefore, TPL2 plays a critical role in regulating the innate immune response. The present review summarizes the recent advancements in the TPL2-regulated innate immune response.

Construction of highly efficient and stable ternary AgBr/Ag/PbBiO2Br Z-scheme photocatalyst under visible light irradiation: Performance and mechanism insight.

In this work, the novel ternary AgBr/Ag/PbBiO2Br Z-scheme photocatalysts were synthesized via a CTAB-assisted calcination process. The AgBr/Ag/PbBiO2Br composites were employed for the degradation of rhodamine B (RhB) and antibiotic bisphenol A (BPA) under visible light irradiation. Results showed that the obtained AgBr/Ag-3/PbBiO2Br displayed optimal photocatalytic performance, which could remove almost all RhB within 25 min and effectively decompose 82.3% of BPA in 120 min. Three-dimensional excitation-emission matrix fluorescence spectra (3D EEMs) were utilized for the purposes of fully grasping the behaviors of RhB molecules during the reaction process. Meanwhile, the effects of initial RhB concentration and co-existent electrolytes were investigated from the viewpoint of practical application. In addition, there was no obvious loss in degradation efficiency even after four cycles. The enhanced photocatalytic performances of AgBr/Ag/PbBiO2Br could be credited to the accelerated interfacial charge transfer process and the improved separation of the photogenerated electron-hole pairs. The existence of a small amount of metallic Ag played a significant role in preventing AgBr from being further photocorroded, resulting in the formation of a stable Z-scheme photocatalyst system. This study demonstrated that using metallic Ag as an electron mediator to construct Z-scheme photocatalytic system provided a feasible strategy in promoting the stability of Ag-based semiconductors.

Graphene sponge decorated with copper nanoparticles as a novel bactericidal filter for inactivation of Escherichia coli.

Nanotechnology has great potential in water purification. However, the limitations such as aggregation and toxicity of nanomaterials have blocked their practical application. In this work, a novel copper nanoparticles-decorated graphene sponge (Cu-GS) was synthesized using a facile hydrothermal method. Cu-GS consisting of three-dimensional (3D) porous graphene network and well-dispersed Cu nanoparticles exhibited high antibacterial efficiency against Esherichia coli when used as a bactericidal filter. The morphological changes determined by scanning electron microscope and fluorescence images measured by flow cytometry confirmed the involvement of membrane damage induced by Cu-GS in their antibacterial process. The oxidative ability of Cu-GS and intercellular reactive oxygen species (ROS) were also determined to elucidate the possible antibacterial mechanism of Cu-GS. Moreover, the concentration of released copper ions from Cu-GS was far below the drinking water standard, and the copper ions also have an effect on the antibacterial activity of Cu-GS. Results suggested that Cu-GS as a novel bactericidal filter possessed a potential application of water disinfection.

Hyaluronic acid and oxidized regenerated cellulose prevent adhesion reformation after adhesiolysis in rat models.

Postsurgical adhesion formation is the most common complication in abdominal and pelvic surgery. Adhesiolysis is the most commonly applied treatment for adhesion formation but is often followed by adhesion reformation. Therefore, an efficient strategy should be adopted to solve these problems. This study aimed to explore whether hyaluronic acid and oxidized regenerated cellulose (ORC) could prevent adhesion formation and reformation. Thirty female Sprague Dawley rats were randomly divided into three groups (n=10 each) and subjected to different treatments during the first and second surgery. The control group was treated with isotonic sodium chloride, the ORC group was treated with ORC (1.5×1 cm), and the medical sodium hyaluronate (MSH) group was treated with 1% MSH (0.5 mL). At 2 weeks after the first surgery, adhesion scores in the MSH group (1.90±0.99) and the ORC group (1.40±0.97) were significantly lower than those in the control group (3.00±0.82) (P=0.005). Similarly, 2 weeks after the second surgery, adhesion scores in the MSH group (2.00±0.82) and the ORC group (1.50±1.27) were significantly lower than those in the control group (3.50±0.53) (P=0.001). In addition, body weights in the MSH group and the ORC group did not change significantly, whereas the control group showed a consistent decrease in body weight during the experiment. Histological examination revealed that inflammatory infiltration was involved in both adhesion formation and reformation. In conclusion, hyaluronic acid and ORC were both efficient in reducing adhesion formation and reformation in the rat model.

A facile "turn-on" fluorescent method with high sensitivity for Hg(2+) detection using magnetic Fe3O4 nanoparticles and hybridization chain reactions.

In this manuscript, the authors molecularly engineered a hybridization chain reactions (HCRs) based probe on magnetic Fe3O4 nanoparticles for the sensitive detection of Hg(2+). The sensing system comprised three probes: capture probe H1, report probe H2, and report probe H3. The capture probe was modified on the surface of magnetic Fe3O4 nanoparticles. The report probes were labeled with fluorescein isothiocyanate (FITC). Without Hg(2+), the report probes were stable as molecular beacons in solution. In the presence of Hg(2+), the T-rich capture probes and report probes will hybridize into double-helical DNA domains with the aid of T-Hg(2+)-T coordination chemistry. Trigged by this reaction, more molecular beacons open and form a super tandem structure. Herein, the fluorescence signal was magnified by capturing more report probes. Separating the target and captured report probes from reaction solution was benefit to decrease the background signal and interference from other metal ions. The detection limit of this method was about 0.36nM, which is much lower than the regulations of World Health Organization and U.S. Environmental Protection Agency on Hg(2+) in drink water. This proposed sensing strategy also showed favorable selectivity over other common metal ions. In addition, it has good practicability in real water samples.

Clinicopathological significance of increased ZIC1 expression in human endometrial cancer.

Zinc finger of the cerebellum (ZIC1), one of ZIC family genes, has been shown to play important roles in many cancers such as gastric cancer and breast cancer. However, there is little known about the expression and significance of ZIC1 in endometrial cancer. The aim of this study was to determine the expression pattern and clinicopathological significance of ZIC1 in endometrial cancer. The mRNA and protein expression of ZIC1 in endometrial cancer tissues was detected using the reverse-transcription polymerase chain reaction and Western blotting, respectively. Immunostaining of ZIC1 in 99 endometrial cancer samples was examined and its associations with clinicopathological parameters were analyzed. Hec-1-B cells were transfected with ZIC1-shRNA or sc-shRNA, and cell proliferation was assayed. Hec-1-B cells stably transfected with ZIC1-shRNA or sc-shRNA were subcutaneously inoculated into nude mice, and the tumor weight was measured. A significantly increased expression of ZIC1 mRNA and protein was observed in endometrial cancer tissues compared to that in normal endometrial tissues (P<0.05). Immunohistochemical analysis showed that strong cytoplasmic immunostaining of ZIC1 was observed in almost all endometrial cancer samples (90/99) while light and moderate immunostaining of ZIC1 was only detected in 17 of 30 (56.7%) normal tissues. Moreover, up-regulation of ZIC1 was significantly correlated with age, disease stage, TNM stage and FIGO stage (P<0.05). The down-regulated expression of ZIC1 contributed to the inhibition of cell proliferation, and inhibited the growth of tumor. It was concluded that ZIC1 is over-expressed in endometrial cancer tissue but not in normal tissue, and positively correlated to the malignant biological behavior of endometrial carcinogenesis.