Prognostic and immunotherapeutic potential of regulatory T cell-associated signature in ovarian cancer.

Tumour-induced immunosuppressive microenvironments facilitate oncogenesis, with regulatory T cells (Tregs) serving as a crucial component. The significance of Treg-associated genes within the context of ovarian cancer (OC) remains elucidated insufficiently. Utilizing single-cell RNA sequencing (scRNA-Seq) for the identification of Treg-specific biomarkers, this investigation employed single-sample gene set enrichment analysis (ssGSEA) for the derivation of a Treg signature score. Weighted gene co-expression network analysis (WGCNA) facilitated the identification of Treg-correlated genes. Machine learning algorithms were employed to determine an optimal prognostic model, subsequently exploring disparities across risk strata in terms of survival outcomes, immunological infiltration, pathway activation and responsiveness to immunotherapy. Through WGCNA, a cohort of 365 Treg-associated genes was discerned, with 70 implicated in the prognostication of OC. A Tregs-associated signature (TAS), synthesized from random survival forest (RSF) and Least Absolute Shrinkage and Selection Operator (LASSO) algorithms, exhibited robust predictive validity across both internal and external cohorts. Low TAS OC patients demonstrated superior survival outcomes, augmented by increased immunological cell infiltration, upregulated immune checkpoint expression, distinct pathway enrichment and differential response to immunotherapeutic interventions. The devised TAS proficiently prognosticates patient outcomes and delineates the immunological milieu within OC, offering a strategic instrument for the clinical stratification and selection of patients.

Real-time detection method for bulk bubbles in optics based on deep learning.

The existence of bulk bubbles could decrease the laser-induced damage threshold of optics and affect the beam quality, so the detection of bulk bubbles is an essential step for quality assurance. Currently, the inspection of bubbles in optics relies on manual work, which is not recommended because of the low precision and inconsistency. To improve the quality evaluation process, a real-time detection method for bubbles inside the optics based on deep learning is proposed. Our method can implement bubble detection at 67 fps with a recall of 0.836. As for retrieval of the radius, it costs 58.8 ms on each bubble, and the absolute deviation is 3.73% on average. Our method conducts real-time and accurate detection of the positions and radii of the bubbles in the optics, thus, having significant potential for the manufacturing process.

MicroRNA-650 suppresses KLF12 expression to regulate growth and metastasis of human ovarian cancer cells.

MicroRNA-650 (miR-650) has been shown to regulate the development of human cancers. The present study investigated the role of miR-650 in ovarian cancer by targeting Krüppel-like factor 12 (KLF12). The results showed a down-regulation of miR-650 in tissues and cell lines. Overexpression of miR-650 caused a substaining decrease in the viability of CAOV3 cells by promoting apoptotic cell death. In silico analysis and dual luciferase assay revealed KLF12 as a potential target of miR-650. Unlike miR-650, KLF12 showed a substantial up-regulation in ovarian cancer tissues and cell lines. However, miR-650 overexpression suppressed KLF12 expression posttranscriptionally. Intrestingly, KLF12 knockdown inhibited the viability of CAOV3 cells by promoting apoptotic cell death. However, the expression of KLF12 eliminated the tumor suppressing effects of miR-650 in CAOV3 cells. Additionally, KLF12 knockdown or miR-650 overexpression suppressed CAOV3 cell migration and invasion. However, KLF12 overexpression eliminated the inhibitory effects of miR-650 on the migration and invasion of CAOV3 cells. Taken together, these results suggest that miR-650/KLF12 axis regulates the viability, migration, and invasion of CAOV3 cells an0d may prove to be an important therapeutic taregt.

Integrated Microarray Analysis to Identify Genes and Small-Molecule Drugs Associated with Stroke Progression.

Several blood biomarkers are now considered increasingly important for stratifying risk, monitoring disease progression, and evaluating the response to therapy in ischemic stroke. The purpose of the present study was to identify the key genes associated with ischemic stroke progression and elucidate the potential therapeutic small molecules. Microarray datasets related to stroke for GSE58294, GSE22255, and GSE16561 were obtained from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were filtered using the Limma package. DAVID was then searched to perform gene ontology (GO) and pathway enrichment analyses. Based on the DEGs, a protein-protein interaction (PPI) network was developed using Cytoscape, and MCODE was applied to conduct module analysis. Finally, to identify the potential drugs for ischemic stroke, the connectivity map (CMap) database was used. Sixty DEGs were identified after analyzing the three datasets. The GO data analysis revealed that the DEGs were significantly associated with biological processes, including positive regulation of programmed cell death, protein localization in organelles, and positive regulation of apoptosis. KEGG analysis showed that the DEGs were particularly enriched in the Fc epsilon RI signaling pathway, MAPK signaling pathway, and Huntington's disease. We selected five DEGs with high connectivity (CYBB, SYK, DUSP1, TNF, and SP1) that significantly predicted stroke progression. In addition, CMap prediction showed ten small molecules that could be used as adjuvants when treating ischemic stroke. The outcomes of the present study indicated that the five genes mentioned above can be considered potential targets for developing new medications that can modify the ischemic stroke process, and mycophenolic acid was the most promising small molecule to treat ischemic stroke.

Association of hyperglycaemia with the placenta of GDM-induced macrosomia with normal pre-pregnancy BMI and the proliferation of trophoblast cells.

The aim of this study was to identify the effect of hyperglycaemia on placentas of gestational diabetes mellitus (GDM) women with macrosomia and normal pre-pregnancy body mass index (BMI), and uncover the molecular mechanism of hyperglycaemia on trophoblast cells in vitro. GDM women with normal pre-pregnancy BMI were divided into GM group (macrosomia, n = 30) and GN group (normal birth weight, n = 35). The study showed GM group had more adverse pregnancy outcomes and higher levels of gestational weight gain, blood glucose and triglyceride. After adjustment for confounding factors, just the fasting plasma glucose level and HbA1c percentage were related to the incidence of GDM-induced macrosomia with normal pre-pregnancy BMI. Meanwhile, the fasting blood glucose was closely related to the placental weight and placental PCNA expression. Furthermore, the in vitro model for placenta showed that hyperglycaemia significantly promoted trophoblast cell proliferation and activated ERK1/2 phosphorylation. ERK1/2 inhibitor markedly suppressed hyperglycaemia-induced trophoblastic proliferation. The fasting plasma glucose and placenta are closely related with the development of GDM-induced macrosomia with normal pre-pregnancy BMI. The mechanism may be hyperglycaemia promotes trophoblast cell proliferation via ERK1/2 signalling. It provides scientific evidence for optimising outcomes of GDM women with normal pre-pregnancy BMI.IMPACT STATEMENTWhat is already known on this subject? Gestational diabetes mellitus (GDM) is one of the strongest risk factors correlated with macrosomia. The hyperglycaemic intrauterine environment affects not only the foetus but also the placental development and function in humans and experimental rodents. However, placental abnormalities associated with maternal diabetes have been inconsistently reported, possibly because of population differences in pre-pregnancy weight, diabetes types, glycemic control or pregnancy complication, and the molecular mechanism of hyperglycaemia on trophoblast cells in vitro was not clearly stated.What do the results of this study add? This is the first study to identify the effect of hyperglycaemia on placentas of gestational diabetes mellitus (GDM) women with macrosomia and normal pre-pregnancy body mass index (BMI), and uncover the molecular mechanism of hyperglycaemia on trophoblast cells in vitro.What are the implications of these findings for clinical practice and/or further research? Understanding placental changes in the environment of abnormal glucose metabolism which can establish the maternal-placental-foetal interface dysfunction as a potential source of adverse pregnancy outcomes is very necessary. Our study found the fasting plasma glucose and placenta are closely related with the development of GDM-induced macrosomia with normal pre-pregnancy BMI. The mechanism may be hyperglycaemia promotes trophoblast cell proliferation via ERK1/2 signalling. It provides scientific evidence for optimising outcomes of GDM women with normal pre-pregnancy BMI, and could be used for the following studies of relationship between placenta and childhood complications.

Polyphyllin E Inhibits Proliferation, Migration and Invasion of Ovarian Cancer Cells by Down-Regulating the AKT/NF-κB Pathway.

Ovarian cancer has long been considered the second-highest cancer threat to women's reproductive system with high mortality. This is ascribed to the absence of highly efficient therapy and cancer metastasis. Accordingly, there is an urgent need for the development of new agents. Recently, Traditional Chinese medicine has gained extensive interest because of its safe use, validity, and distinct pharmacological effects. Polyphyllin E (PPE), as a major constituent in Rhizoma Paridis, is a promising cancer-fighting agent. However, the effect of PPE on ovarian cancers as well as associated latent mechanisms is still not completely understood. In this study, PPE was found to prohibit the proliferation of SK-OV-3 and OVCAR-3 ovarian cancer cells, causing marked cell death. Additionally, low-dose PPE could also inhibit motility and invasion of ovarian cancer cells. The mechanistic assessment revealed PPE-mediated matrix metalloproteinases, i.e., MMP2 and MMP9, inhibition via the AKT-nuclear factor kappa B (AKT/NF-κB) signaling pathway. Rescue experiments with transfection of AKT lentiviral particles remarkably reversed PPE inhibitory effects against ovarian cancer cells. In conclusion, PPE could inhibit proliferation of ovarian cancer cell migration and invasion by down-regulating the AKT/NF-κB pathway. Moreover, it has the potential to act as a novel agent for ovarian cancer treatment.

LINC00184 Promotes Ovarian Cancer Cells Proliferation and Cisplatin Resistance by Elevating CNTN1 Expression via Sponging miR-1305.

OBJECTIVE: Cisplatin resistance is one of the main reasons for treatment failure in ovarian cancer (OC). Here, the effects of LINC00184 on cisplatin-resistant OC were studied. PATIENTS AND METHODS: LINC00184, miR-1305 and CNTN1 expression in tissues from 70 OC patients was determined by qRT-PCR, in situ hybridization and Western blot. OC cell lines and OC cisplatin-resistant cell lines were cultured. Cells were transfected using Lipofectamine 2000 and treated with 100 nM cisplatin. Cell proliferation and apoptosis were researched by the CCK-8 assay and flow cytometry. A dual-luciferase reporter gene assay and RNA pull-down were performed to explore the relationship between two genes. LINC00184, miR-1305 and CNTN1 expression in cells was detected by qRT-PCR and Western blot. An in vivo experiment was conducted using nude mice. Ki67 and CNTN1 expression and apoptosis of xenograft tumors were investigated using immunohistochemistry and a TUNEL assay. RESULTS: LINC00184 was up-regulated in OC clinical tissues and OC cells, especially in cisplatin-resistant OC patients and cells (p<0.01 or p<0.0001). LINC00184 overexpression significantly enhanced OC cell proliferation and cisplatin resistance, and inhibited OC cell apoptosis (p<0.05 or p<0.01). LINC00184 elevated CNTN1 expression via sponging miR-1305. LINC00184 overexpression markedly exacerbated the malignant phenotype of OC cells and cisplatin-resistant OC cells via the miR-1305/CNTN1 axis (p<0.01). Silencing of LINC00184 significantly suppressed OC cell growth and cisplatin resistance in vivo (p<0.01). LINC00184 silencing inhibited Ki67 and CNTN1 expression and promoted apoptosis of xenograft tumors. CNTN1 overexpression promoted proliferation and cisplatin resistance, and reduced apoptosis of OC cells (p<0.05 or p<0.01). CONCLUSION: LINC00184 promoted OC cell proliferation and cisplatin resistance by elevating CNTN1 expression via sponging miR-1305.

Profiling of MicroRNAs and Their Targets in Roots and Shoots Reveals a Potential MiRNA-Mediated Interaction Network in Response to Phosphate Deficiency in the Forestry Tree Betula luminifera.

Inorganic phosphate (Pi) is often lacking in natural and agro-climatic environments, which impedes the growth of economically important woody species. Plants have developed strategies to cope with low Pi (LP) availability. MicroRNAs (miRNAs) play important roles in responses to abiotic stresses, including nutrition stress, by regulating target gene expression. However, the miRNA-mediated regulation of these adaptive responses and their underlying coordinating signals are still poorly understood in forestry trees such as Betula luminifera. Transcriptomic libraries, small RNA (sRNA) libraries, and a mixed degradome cDNA library of B. luminifera roots and shoots treated under LP and normal conditions (CK) were constructed and sequenced using next-generation deep sequencing. A comprehensive B. luminifera transcriptome derived from its roots and shoots was constructed, and a total of 76,899 unigenes were generated. Analysis of the transcriptome identified 8,095 and 5,584 differentially expressed genes in roots and shoots, respectively, under LP conditions. sRNA sequencing analyses indicated that 66 and 60 miRNAs were differentially expressed in roots and shoots, respectively, under LP conditions. A total of 109 and 112 miRNA-target pairs were further validated in the roots and shoots, respectively, using degradome sequencing. Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis of differential miRNA targets indicated that the "ascorbate and aldarate metabolism" pathway responded to LP, suggesting miRNA-target pairs might participating in the removing of reactive oxidative species under LP stress. Moreover, a putative network of miRNA-target interactions involved in responses to LP stress in B. luminifera is proposed. Taken together, these findings provide useful information to decipher miRNA functions and establish a framework for exploring P signaling networks regulated by miRNAs in B. luminifera and other woody plants. It may provide new insights into the genetic engineering of high use efficiency of Pi in forestry trees.

Constructing Strong Interfacial Interactions under Mild Conditions in MOF-Incorporated Mixed Matrix Membranes for Gas Separation.

Although mixed matrix membranes (MMM) possess remarkably improved gas separation performance compared to traditional polymeric membranes, membrane stability including CO2 plasticization and aging is still a serious issue due to the existence of interfacial defects. In this work, we report an efficient and less destructive route to cross-link the MOFs/polyimide (PI) MMM, where amine group-functionalized MOF (NH2-UiO-66) nanoparticles are thermally cross-linked with a carboxylic acid-functionalized PI (COOH-PI) matrix to form an amide bond at the interface at 150 °C under vacuum condition. Such a chemical cross-linking strategy conducted at a relatively mild condition improves membrane stability greatly while ensuring that the membrane structure is not destroyed. The resulting cross-linked MMM achieves enhanced mechanical strength with higher Young's modulus than a pristine polymer membrane. The CO2 antiplasticization pressure of the MMM after cross-linking is enhanced by 200% from ∼10 to >30 bar and the CO2 permeability of MMM only drops slightly from 995 to 735 Barrer after 450 days. At the same time, the separation performance of H2/CH4 gas pair surpasses the 2008 upper bound and that of CO2/CH4 gas pair nearly approaches the 2008 upper bound. The cross-linking strategy used herein provides a feasible and effective route for improving membrane stability and membrane performance in the MMM system for gas separation.

Effects on Carbon Molecular Sieve Membrane Properties for a Precursor Polyimide with Simultaneous Flatness and Contortion in the Repeat Unit.

Carbon molecular sieve (CMS)-based membrane separation is a promising solution for hydrogen separation due to its great advantages on perm-selectivity, thermal stability, and chemical stability. To prepare high-performance CMS membranes, the molecular structure of polymer precursors and their arrangements should be primarily considered. In this work, a benzimidazole-based 6FDA (2,2'-bis(3,4'-dicarboxyphenyl) hexafluoropropane dianhydride)-type polyimide (PABZ-6FDA-PI) is chosen as precursor to prepare the CMS membrane. Effects of chain flatness and contortion in the polyimide precursor on gas-separation performance of CMS membranes were studied in detail by gas adsorption and permeation experiment. The H2 permeability of CMS is up to 9500 Barrer and ideal selectivity of gas pairs of H2 /CH4 and H2 /CO2 is up to 3800 and 13, respectively. The comprehensive performance of hydrogen separation including H2 /CO2 , H2 /N2 , and H2 /CH4 gas pairs is located well above previously reported upper bounds for polymers.

Effects of the crystallinity on quercetin loaded the Eudragit L-100 electrospun nanofibers.

The quercetin loaded Eudragit L-100 nanofiber membrane with high ductility and a desired drug release rate was prepared in this work. The morphological characteristics of the Eudragit L-100 nanofibers with different drug loadings amount were observed by scanning electron microscope (SEM). After adding Polyethylene glycol-4000 (PEG-4000), the degree of the fiber breakage decreased and the fiber length increased. Fiber diameter analysis, X-ray diffraction (XRD), thermal analysis (TA) and differential scanning calorimetry (DSC) have demonstrated that the crystallinity of the fiber membrane was significantly reduced after adding PEG-4000. The mechanical property test also showed that the fiber membrane with PEG-4000 had a greater elongation at break. The in vitro release experiments showed that after adding PEG-4000, the drug-loaded fibers showed rapid release at a pH of 7.4. After adopting the strategy of reducing the crystallinity, the ductility of the fiber was enhanced, which could provide a fesibility to enable this nanofiber membrane to be used in sports wound healing treatment. The electrospun Eudragit L-100 nanofiber membranes loaded with quercetin have the potential to be applied in sport wound healing of skin, tissue and joints.

Two-Dimensional Microporous Material-based Mixed Matrix Membranes for Gas Separation.

Since the discovery of graphene and its derivatives, the development and application of two-dimensional (2D) materials have attracted enormous attention. 2D microporous materials, such as metal-organic frameworks (MOFs), covalent organic frameworks (COFs), graphitic carbon nitride (g-C3 N4 ) and so on, hold great potential to be used in gas separation membranes because of their high aspect ratio and homogeneously distributed nanometer pores, which are beneficial for improving gas permeability and selectivity. This review briefly summarizes the recent design and fabrication of 2D microporous materials, as well as their applications in mixed matrix membranes (MMMs) for gas separation. The enhanced separation performances of the membranes and their long-term stability are also introduced. Challenges and the latest development of newly synthesized 2D microporous materials are finally discussed to foresee the potential opportunities for 2D microporous material-based MMMs.

c-Yes enhances tumor migration and invasion via PI3K/AKT pathway in epithelial ovarian cancer.

Overexpression of c-Yes has been noted to correlation with several human cancers. However, the effects of c-Yes on epithelial ovarian cancer (EOC) development remain unclear. The aim of this study is going to prove the effects of c-Yes and related mechanisms in proliferation, metastasis and invasion of EOC. Immunohistochemical analysis was performed in 119 human EOC samples, and the data was correlated with clinic pathologic features. Furthermore, western blot analysis is performed for c-Yes in EOC samples and cell lines to evaluate their protein levels and molecular interaction. Kaplan-Meier survival analysis shows that the strong expression of c-Yes exhibited a significant correlation with poor prognosis in human EOC (P<0.01(⁎)). Meanwhile, we found that knockdown of c-Yes by shRNA inhibited the ability of migration and invasion in EOC cells via the PI3K/AKT pathway. In a word, these results suggested that c-Yes plays an important role in migration and invasion of EOC.

[Expression analysis of miR164 and its target gene NAC1 in response to low nitrate availability in Betula luminifera].

Nitrogen, an essential macronutrient for the growth and development of plants, affects above- ground biomass accumulation dramatically. Thus, it is very important to reveal the molecular mechanisms of how plants resist or adapt to low nitrogen availability. The NAC1(NAM, ATAF, CUC 1) gene, located in the upstream regulatory network, has been reported to resist low nitrogen by regulating expression of key downstream genes and thus root growth in (Populus tremula × alba).In this study, we detected the responses of miR164 and its target gene NAC1 under nitrate-starvation condition using the Betula luminifera somaclones G49-3 as material. The NAC1 gene which contains 1497 bp sequence, encodes 358 amino acids and contains a highly conserved NAM domain at N terminal was cloned by the RACE method. The NAC1 was then validated to be the target gene of miR164 via 5'-RACE, and the cleavage site was between the 10(th) and 11(th) base. The expression patterns of miR164 and its target gene NAC1 were further detected under nitrate-starvation condition through qRT-PCR analysis. The results showed that miR164 expression was repressed by nitrate-starvation at the beginning of the treatment (4 d) and then ascended. However, the expression pattern of miR164 in roots was different from that in shoots and leaves. Moreover, the expression levels of target gene NAC1 and miR164 were negatively correlated. The expression level of miR164 in root was increased while that of NAC1 was decreased under Re treatment, which indicated that miR164 and its target gene NAC1 play a regulatory role in response to low nitrate availability. The findings of our study may help elucidate the molecular mechanisms by which miR164 regulates target gene NAC1 at post-transcriptional level, and provide valuable information for further study of the regulatory roles of miR164-NAC1 under nitrate-starvation condition.

High expression of CDC6 is associated with accelerated cell proliferation and poor prognosis of epithelial ovarian cancer.

Cell division cycle 6 (CDC6) is an essential regulator of DNA replication and plays important roles in the activation and maintenance of the checkpoint mechanisms in the cell cycle. CDC6 has been associated with the oncogenic activities in human cancers, but the biological function and clinical significance of CDC6 in EOC remain unclear. The aim of the present study is to examine the effect of CDC6 on epithelial ovarian cancer (EOC) cells proliferation. We found that CDC6 protein level was up-regulated in EOC tissues compared with the normal ovary tissues. CDC6 expression correlated significantly with FIGO stage (p<0.001), differentiation grade (p=0.002), ascites (p<0.001), malignant tumor cells in ascites (p=0.004), and lymph node status (p<0.001). In vitro, after the release of ovarian cancer cell line (HO8910) from serum starvation, the expression of CDC6, cyclinD1, and PCNA was up-regulated, whereas p16 expression was down-regulated. Furthermore, down-regulation of CDC6 in HO8910 cells decreased cell proliferation and colony formation. HO8910 cells transfected with sh CDC6#1 underwent G1 phase cell cycle arrest. Collectively, this study provides a novel regulatory signaling pathway of CDC6-regulated EOC growth and a new potential therapeutic target for EOC patients.

The role of Cyclin G1 in cellular proliferation and apoptosis of human epithelial ovarian cancer.

Cyclin G1 plays an essential role in the development of human carcinoma. Here, we characterized the clinical significance of Cyclin G1 and investigated its role in cellular proliferation and apoptosis of epithelial ovarian cancer (EOC). Western blot was used to evaluate the expression of Cyclin G1 in nine fresh EOC tissues and three fresh normal ovarian tissues. Immunohistochemistry analysis was performed on formalin-fixed paraffin-embedded section of 119 cases of EOCs. Using cell counting kit (CCK)-8 and colony formation assays, we analyzed the effect of Cyclin G1 in cellular proliferation of EOC. Besides, the immunofluorescence and flow cytometry analysis was performed to study the role of Cyclin G1 in cellular apoptosis of EOC. We found Cyclin G1 was up-regulated in EOC tissues compared with the normal ovary tissues. Cyclin G1 expression in EOC was closely correlated with differentiation grade (P = 0.009) and malignant tumor cells in ascites (P = 0.009). The Kaplan-Meier curve showed that higher expression of Cyclin G1 was associated with significantly shorter survival in EOC patients. Multivariate analysis suggested Cyclin G1 expression was an independent prognostic factor for overall survival. CCK-8 and colony formation assays revealed that depletion of Cyclin G1 inhibited the proliferation and clone formation. Combined immunofluorescence and flow cytometry analysis showed that silencing of Cyclin G1 with shRNA could promote apoptosis of ovarian cancer cells. Additionally, the result of immunoprecipitation test showed Cyclin G1 interacted with CDK2 in EOC cells. In summary, our findings suggest that Cyclin G1 may be involved in the prognosis of EOC patients and be a useful therapeutic target for EOC.

The expression of CDK1 is associated with proliferation and can be a prognostic factor in epithelial ovarian cancer.

Overexpression of cyclin-dependent kinase 1 (CDK1) has been noted to correlation with several human cancers. However, the effects of CDK1 on ovarian cancer development remain unclear. The aim of this study was to examine the effect of CDK1 and related mechanism in the proliferation and resistance to chemotherapeutic drugs of epithelial ovarian cancer (EOC). Immunohistochemical analysis was performed in 119 human ovarian cancer samples, and the data were correlated with clinicopathologic features. Furthermore, Western blot analysis was performed for CDK1 in EOC samples and cell lines to evaluate their protein levels and molecular interaction. Kaplan-Meier survival analysis showed that strong expression of CDK1 exhibited a significant correlation with poor prognosis in human EOC (P = 0.02). Meanwhile, we found that knockdown CDK1 by shCDK1 promoted the apoptosis rate and increased the sensitivity to chemotherapy drugs. Thus, CDK1 might serve as a prognostic marker, and it might be of great value for experimental therapies in EOC.

Ubiquitin-specific protease 14 (USP14) regulates cellular proliferation and apoptosis in epithelial ovarian cancer.

Epithelial ovarian cancer (EOC) is the most lethal gynecologic malignancy. Thus, there is an emergent need to invest a novel therapeutic for EOC. In this study, we defined ubiquitin-specific protease 14 (USP14) as a therapeutic target for EOC. Western blot was used to evaluate the expression of USP14 in nine fresh EOC tissues and three fresh normal ovarian tissues. The protein level of USP14 was higher in the cancer samples compared with that in the normal ovary tissues. Immunohistochemistry analysis was performed on formalin-fixed paraffin-embedded section of 116 cases of EOCs and indicated that USP14 was significantly associated with clinical pathologic variables. Kaplan-Meier curve showed that high expression of USP14 was related to poor prognosis of EOC patients. Starvation and re-feeding assay was used to imitate cell cycle, suggesting that USP14 played a critical role in SKOV3 cell proliferation. CCK-8 assay showed that SKOV3 cells treated with USP14-shRNA (shUSP14) grew more slowly than control group. Flow cytometry revealed that the reduced expression of USP14 induced the apoptosis of the SKOV3 EOC cells. In summary, our findings suggest that USP14 is involved in the progression of EOC and that it may be a useful target of therapy in EOC.