Seven drimane-type sesquiterpenoids from an earwig-associated Aspergillus sp.

Drimane-type sesquiterpenoids are widely distributed in fungi. From the ethyl acetate extract of the earwig-derived Aspergillus sp. NF2396, seven new drimane-type sesquiterpenoids, named drimanenoids A-G (1-7), were isolated. Their structures were elucidated by diverse spectroscopic analysis including high-resolution ESI-MS, one- and two-dimensional NMR spectroscopy. Drimanenoids A-F (1-6) are new members of drimane-type sesquiterpenoid esterified with unsaturated fatty acid side chain at C-6. Drimanenoids C (3), D (4) and F (6) showed antibacterial activity against five types of bacteria with different inhibition diameters. Drimanenoid D (4) exhibited moderate cytotoxicity against human myelogenous leukemia cell line K562 with an IC50 value of 12.88 ± 0.11 µmol·L-1.

New metabolites from Streptomyces pseudovenezuelae NA07424 and their potential activity of inducing resistance in plants against Phytophthora capsici.

BACKGROUND: The lack of novel fungicide and appearance of resistance are the most emergent problems in the control of Phytophthora diseases. Plant immunity elicitors that induce systemic resistance in plants are regarded as the new strategy for plant disease control. Streptomyces can produce a variety of bioactive natural products, which are important resources for lead compounds of plant immunity elicitors. RESULTS: A novel peptidendrocin C (1) together with the known analog peptidendrocin B (2) were isolated from Streptomyces pseudovenezuelae NA07424. Their structures were confirmed by spectroscopic data and Marfey's reaction. In bioactive assays, compound 1 played an important role in inducing systemic resistance of Nicotiana benthamiana against Phytophthora capsici growth, with a 90.5% inhibition ratio at 400 µg/mL, while compound 2 showed moderate activity, inhibiting P. capsici growth by a 50.8% decrease at 400 µg/mL. Simultaneously, two compounds promoted enhanced expression of the PR1 gene and callose accumulation in N. benthamiana and Arabidopsis thaliana. In this paper, we also provide the first insights into their biosynthesis by confirming their biosynthesis gene cluster and related functional genes. CONCLUSION: Our findings show that 1 and 2 have the potential to be used as lead compounds for development of new plant immunity elicitors to control Phytophthora diseases. The study of the biosynthesis pathway lays the groundwork for further application of the bioactive natural products. © 2022 Society of Chemical Industry.

Identification of key genes and miRNAs related to polycystic ovary syndrome by comprehensive analysis of microarray.

BACKGROUND: We aimed to explore mechanisms of development and progression of polycystic ovary syndrome (PCOS). METHODS: The microRNA expression microarray GSE37914 and gene expression profiles GSE43264 and GSE98421 were downloaded from the Gene Expression Omnibus database. The differentially expressed miRNAs (DEmiRNAs) and genes (DEGs) were screened using Limma package. Then, the DEGs and DEmiRNAs were combined to use for the subsequent analysis, including the functional enrichment analysis, protein-protein interaction (PPI) network and module analysis, drug-gene interaction network analysis, and DEmiRNAs-DEGs interactive network construction. RESULTS: A total of 26 DEmiRNAs and 80 DEGs were screened. The PPI network contained 68 nodes and 259 interactions. A significant clustering module with 8 nodes and 25 interactions was obtained. Three PCOS-related overlapping pathways were obtained based on PPI-degree top10 and module genes, including prion diseases, Staphylococcus aureus infection, and Chagas disease (American trypanosomiasis). A total of 44 drug-gene interaction pairs were obtained, which included 2 up-regulated genes (LDLR and VCAM1), 4 down-regulated genes (C1QA, C1QB, IL6 and ACAN) and 26 small molecules drugs. A total of 52 nodes and 57 interactions were obtained in the DEmiRNA-DEGs regulatory network, LDLR was regulated by miR-152-3p, miR-1207-5p, miR-378a-5p and miR-150-5p. CONCLUSIONS: Our research has identified several key genes and pathways related to PCOS. These results can improve our understanding of PCOS and provide new basis for drug target research.

Auto-Continuous Synthesis of Robust and Hydrophobic Silica Aerogel Microspheres from Low-Cost Aqueous Sodium Silicate for Fast Dynamic Organics Removal.

An efficient auto-continuous globing process was developed with a self-built apparatus to synthesize pure silica aerogel microspheres (PSAMs) using sodium silicate as a precursor and water as a solvent. A hydrophobic silica aerogel microsphere (HSAM) was obtained by methyl grafting. A reinforced silica aerogel microsphere (RSAM) was prepared by polymer cross-linking on the framework of the silica gel. The pH value of the reaction system and the temperature of the coagulating bath were critical to form perfect SAMs with a diameter of 3.0 ± 0.2 mm. The grafted methyl groups are thermally stable up to 400 °C. Polymer cross-linking increased the strength significantly, owing to the polymer coating on the framework of silica aerogel. The pore volumes of HSAM (6.44 cm3/g) and RSAM (3.17 cm3/g) were much higher than their state-of-the-art counterparts. Their specific surface areas were also at a high level. The HSAM and RSAM showed high organic sorption capacities, i.e., 17.9 g/g of pump oil, 11.8 g/g of hexane, and 22.2 mg/g of 10 mg/L methyl orange. The novel preparation method was facile, cost-effective, safe, and eco-friendly, and the resulting SAM sorbents were exceptional in capacity, dynamics, regenerability, and stability.

Effect of knee joint weight change on knee function recovery and gait after total knee arthroplasty.

BACKGROUND: Knee osteoarthritis (KOA) is a common disease based on degenerative pathological changes. Total knee arthroplasty (TKA) is an effective treatment for end-stage of KOA. However, only volume adaptation can be achieved with current knee prostheses, and it is difficult to achieve weight adaptation. This study focused on the weight difference of knee joints and initially explored the impact of this change on knee joint functional recovery and gait changes in patients after surgery. METHODS: From October 2015 to June 2019, patients who underwent primary unilateral TKA were enrolled in this prospective cohort study with the same brand of knee prostheses. General data were collected from patients who met the criteria. The resected bone and soft tissues were collected and weighed precisely during TKA, and multivariate regression analysis was used to determine the factors affecting the weight of the removed knee tissues. We compared the weight of excised tissues and the total weight of the knee prosthesis, and the weight difference was defined as the increased weight of the knee joint (IWKJ). All patients were evaluated by HSS score, gait analysis, and affected side knee X-ray at two weeks, three months, and the last follow-up after the operation. To further determine the influence of IWKJ on postoperative functional recovery, the relationship between IWKJ, HSS score, and gait analysis was analyzed by univariate regression. RESULTS: In total, 210 patients were eventually included in observation. All patients underwent postoperative follow-up for no less than two years. Multiple regression analysis showed that the course of the disease, body weight, and kellgren-Larencen stage(K-L stage)of the affected knee joint were independent factors affecting the weight of the removed knee tissues and were positively correlated with it. Univariate analysis showed that IWKJ was negatively correlated with HSS score at two weeks and three months after the operation. In addition, the values of spatiotemporal parameters and knee rotation ROM were negatively correlated with IWKJ two weeks after surgery, while outside food load response was positively correlated with IWKJ. Cadence, knee rotation ROM, and Ankle rotation ROM were negatively correlated with IWKJ, while outside food was positively correlated with IWKJ three months after surgery. At the last follow-up, only the hip rotation ROM was positively correlated with IWKJ. CONCLUSIONS: All Patients underwent TKA had varying degrees of increased knee weight. The increased weight was 298.98 ± 63.77 g. Patients' body weight, K-L staging, and disease duration are important factors that cause differences in resected knee tissue. Three months after the operation, the changes in knee joint weight had a negative correlation with the HSS score, which at the same time, it had varying degrees of linearity with gait parameters. However, the influence of weight diminished over time.

Screening of genes related to survival prognosis of cervical squamous cell carcinoma and construction of prognosis prediction model.

AIM: We aimed to screen for the genes related to survival prognosis of cervical squamous cell carcinoma (CSCC) and then constructed a prognosis prediction model. METHODS: The GSE63514 dataset was obtained from the National Center for Biotechnology Information (NCBI) Gene Expression Omnibus (GEO). The CSCC gene dataset and the GSE44001 dataset were obtained from The Cancer Genome Atlas and NCBI GEO, respectively. The Kaplan-Meier (KM) curve was used to evaluate the association between high and low prognosis that was with the actual survival prognosis information. The Cox proportional hazards model was used to screen out the optimized prognostic-related signature differentially expressed gene (DEG) combinations. Gene set enrichment analysis was used to perform pathway enrichment annotation analysis for DEGs that were related to risk grouping. RESULTS: In total, 16 399 DEGs were obtained and 23 gene ontology biological processes and 8 Kyoto Encyclopedia of Genes and Genomes pathways were screened. Nine optimized DEG groups related to independent prognosis were selected. The KM curves of pathologic N0 and N1 showed that low-risk group were associated with a better overall survival (p = 1.518e; p = 1.704e-01). The pathways related to risk grouping were cytokine-cytokine receptor interaction, JAK stat signaling pathway, and glycolysis-gluconeogenesis. CONCLUSION: On the basis of this study, we established a prognostic risk model, which provided a reliable prognostic tool and was of great significance for locating the biomarkers related to survival prognosis in CSCC.

Silencing LINC01021 inhibits gastric cancer through upregulation of KISS1 expression by blocking CDK2-dependent phosphorylation of CDX2.

Gastric cancer remains one of the most dangerous cancers, bringing suffering and economic burden to people worldwide. Long noncoding RNAs (lncRNAs) exhibit great potentials for targeted therapy of various cancers. In this investigation, we tested mechanisms by which LINC01021 may regulate gastric cancer progression. We collected gastric cancer tissues and procured cell lines to explore the potential factors by which LINC01021 had effects on angiogenesis, invasion, and migration, by quantitative reverse-transcription polymerase chain reaction (qRT-PCR), Transwell assay, and western blot analysis. Relationships among LINC01021, Caudal-type homeobox 2 (CDX2), and KISS1 were validated by dual-luciferase gene reporter, RNA pull-down, and RNA immunoprecipitation assays. Additionally, a murine model was developed to further explore the impact of LINC01021 on tumors in vivo. LINC01021 was upregulated in gastric cancer tissues and cells. LINC01021 regulated KISS1 through CDK2, which promoted phosphorylation and nuclear export in CDX2. Inhibition of LINC01021 suppressed the tumorigenesis of gastric cancer. Further, silencing LINC01021 exerted an inhibitory effect on cancer cell migration, invasion, and angiogenesis by promoting the binding between CDX2 and KISS1, while inhibiting that between CDK2 and CDX2. Taken altogether, high LINC01021 expression in gastric cancer promotes malignant cell migration and angiogenesis by downregulation of KISS1 through CDK2-mediated CDX2 phosphorylation.

A novel prognostic prediction model based on seven immune-related RNAs for predicting overall survival of patients in early cervical squamous cell carcinoma.

BACKGROUND: In this study, we aimed to mine immune-related RNAs expressed in early cervical squamous cell carcinoma to construct prognostic prediction models. METHODS: The RNA sequencing data of 309 cervical squamous cell carcinoma (CSCC) cases, including data of individuals with available clinical information, were obtained from The Cancer Genome Atlas (TCGA) database. We included 181 early-stage CSCC tumor samples with clinical survival and prognosis information (training dataset). Then, we downloaded the GSE44001 gene expression profile data from the National Center for Biotechnology Information Gene Expression Omnibus (validation dataset). Gene ontology annotation and the Kyoto Encyclopedia of Genes and Genomes pathway analyses were used to analyze the biological functions of differentially expressed immune-related genes (DEIRGs). We established protein-protein interactions and competing endogenous RNA networks using Cytoscape. Using the Kaplan-Meier method, we evaluated the association between the high- and low-risk groups and the actual survival and prognosis information. Our univariate and multivariate Cox regression analyses screened for independent prognostic factors. RESULTS: We identified seven prognosis-related signature genes (RBAKDN, CXCL2, ZAP70, CLEC2D, CD27, KLRB1, VCAM1), the expression of which was markedly associated with overall survival (OS) in CSCC patients. Also, the risk score of the seven-gene signature discripted superior ability to categorize CSCC patients into high-risk and low-risk groups, with a observablydifferent OS in the training and validation datasets. We screened two independent prognostic factors (Pathologic N and prognostic score model status) that correlated significantly by univariate and multivariate Cox regression analyses in the TCGA dataset. To further explore the potential mechanism of immune-related genes, we observed associated essential high-risk genes with a cytokine-cytokine receptor interaction. CONCLUSIONS: This study established an immune-related RNA signature, which provided a reliable prognostic tool and may be of great significance for determining immune-related biomarkers in CSCC.

Astragaloside IV antagonizes M2 phenotype macrophage polarization-evoked ovarian cancer cell malignant progression by suppressing the HMGB1-TLR4 axis.

Macrophages are the most abundant cells in tumor stroma and their polarization within tumor microenvironment exert the key roles in tumorigenesis. Astragaloside IV is a natural extract from traditional Chinese herbal Radix Astragali, and fulfills pleiotropic function in several cancers. Nevertheless, its function in ovarian cancer microenvironment remains elusive. In the present research, astragaloside IV exhibited little cytotoxicity within a certain dose range in THP-1 cells. Moreover, astragaloside IV suppressed the ratio of CD14+CD206+ cells in IL-4/IL-13-treated THP-1 macrophages and transcripts of M2 macrophage markers (including CD206, CCL24, PPARγ, Arg-1, IL-10), indicating the inhibitory effects of astragaloside IV on IL-4/IL-13-induced macrophage M2 polarization. Intriguingly, astragaloside IV antagonized M2 macrophages coculture-evoked cell proliferation, invasion and migration in ovarian cancer cells. During this process, administration with astragaloside IV restrained the high expression of high-mobility group box1 (HMGB1) and TLR4 in macrophages co-cultured with ovarian cancer cells, concomitant with decreases in release of M2 marker TGF-ß, MMP-9 and IL-10. Moreover, targeting the HMGB1 signaling reversed M2 macrophages-induced ovarian cancer cell proliferation, invasion and migration. Noticeably, exogenous HMGB1 overturned the inhibitory efficacy of astragaloside IV against macrophage M2 polarization-evoked malignant potential in ovarian cancer cells. Together, these findings suggest that astragaloside IV may protect against M2 macrophages-evoked malignancy in ovarian cancer cells by suppressing the HMGB1-TLR4 signaling. Therefore, astragaloside may alleviate the progression of ovarian cancer by regulating macrophage M2 polarization within tumor microenvironment, implying a promising therapeutic strategy against ovarian cancer.

hsa_circ_001653 up-regulates NR6A1 expression and elicits gastric cancer progression by binding to microRNA-377.

NEW FINDINGS: What is the central question of this study? Does hsa_circ_001653 influence the development of gastric cancer (GC) and if so how? What is the main finding and its importance? Bioinformatics analysis revealed the presence of differentially expressed hsa_circ_001653 in GC and adjacent normal tissues, and this was strongly related to the pathology of patients with GC. Knockdown of hsa_circ_001653 suppressed the proliferation, invasion and migration of GC cells, while inducing cell apoptosis via miR-377-mediated NR6A1 inhibition. The effect of hsa_circ_001653 and miR-377 on tumour growth in GC was further confirmed in vivo. ABSTRACT: Gastric cancer (GC) is one of the leading causes of human mortality through malignant tumours. Circular RNAs (circRNAs) have been identified as binding to microRNAs (miRNAs) to modulate the progression of tumours. This study explores the role of hsa_circ_001653, a newly identified circRNA, in the development of GC. hsa_circ_001653 expression was measured in 86 paired normal and tumour tissues surgically resected from GC patients. Cross-talk between hsa_circ_001653 and microRNA-377 (miR-377)/nuclear receptor subfamily 6, group A, member 1 (NR6A1) was assessed using bioinformatics analysis, dual-luciferase reporter assay, Ago2 immunoprecipitation and western blot analysis. A series of functional experiments were carried out to elucidate the role of hsa_circ_001653 in GC cell proliferation, invasion, migration and apoptosis, and its underlying molecular mechanisms. Nude mice were inoculated with GC cells for in vivo analysis. hsa_circ_001653 was found to be an up-regulated circRNA in GC tissues and cells. Down-regulation of hsa_circ_001653 inhibited GC cell proliferation, migration and invasion, while stimulating cell apoptosis. hsa_circ_001653 was found to bind to miR-377, which targeted NR6A1 and repressed its expression. Inhibition of miR-377 and overexpression of NR6A1 restored the proliferation, migration and invasion in GC cells lacking hsa_circ_001653. Furthermore, inhibition of hsa_circ_001653 attenuated tumour growth in nude mice inoculated with GC cells. Collectively, the demonstration that hsa_circ_001653 exerts its anticancer effects by regulating the miR-377-NR6A1 axis increases our understanding of gastric cancer pathophysiology. The findings uncover new potential therapeutic targets for GC.

Long non-coding RNA FEZF1-AS1 induced progression of ovarian cancer via regulating miR-130a-5p/SOX4 axis.

Emerging studies have revealed the critical role of long non-coding RNAs (lncRNAs) in epithelial ovarian cancer (EOC) development and progression. Till now, the roles and potential mechanisms regarding FEZF1 antisense RNA 1 (FEZF1-AS1) within ovarian cancer (OC) remain unclear. The objective of this study was to uncover the biological function and the underlying mechanism of LncRNA FEZF1-AS1 in OC progression. FEZF1-AS1 expression levels were studied in cell lines and tissues of human ovarian cancer. In vitro studies were performed to evaluate the impact of FEZF1-AS1 knock-down on the proliferation, invasion, migration and apoptosis of OC cells. Interactions of FEZF1-AS1 and its target genes were identified by luciferase reporter assays. Our data showed overexpression of FEZF1-AS1 in OC cell lines and tissues. Cell migration, proliferation, invasion, wound healing and colony formation were suppressed by silencing of FEZF1-AS1. In contrast, cell apoptosis was promoted by FEZF1-AS1 knock-down in vitro. Furthermore, online bioinformatics analysis and tools suggested that FEZF1-AS1 directly bound to miR-130a-5p and suppressed its expression. Moreover, the inhibitory effects of miR-130a-5p on the OC cell growth were reversed by FEZF1-AS1 overexpression, which was associated with the increase in SOX4 expression. In conclusion, our results revealed that FEZF1-AS1 promoted the metastasis and proliferation of OC cells by targeting miR-130a-5p and its downstream SOX4 expression.

Low BCL7A expression predicts poor prognosis in ovarian cancer.

BACKGROUND AND OBJECTIVE: Ovarian cancer is a common gynaecological cancer with a poor prognosis that poses a serious threat to human life and health. It is essential to explore the possible prognostic biomarkers of ovarian cancer. As an important tumour suppressor gene, BCL7A actively participates in the growth of tumours. We aimed to study the prognostic role of BCL7A in ovarian cancer. RESULTS: Through data mining of RNAseq data from the Cancer Genome Atlas database (TCGA), we explored the clinical relevance of BCL7A mRNA expression. As a result, we found that BCL7A is expressed at low levels in ovarian cancer tissues and is correlated with survival status. Survival analysis showed that, compared with those who had higher levels of BCL7A expression, patients with ovarian cancer and low levels of BCL7A generally had shorter overall/relapse-free survival times. Cox regression models showed that low BCL7A expression could be used as an independent prognostication factor for ovarian cancer patients. CONCLUSIONS: Low BCL7A expression is an independent risk factor for poor prognosis in ovarian cancer patients.

Efficacy and tolerability of fluvoxamine in adults with social anxiety disorder: A meta-analysis.

BACKGROUND: No meta-analysis for estimating the comprehensive efficacy and tolerability of fluvoxamine in patients with social anxiety disorder (SAD) has been published. OBJECTIVE: To investigate the efficacy and tolerability of fluvoxamine in adults with SAD, trials meeting the following criteria were identified: population: ≥18 years of age with a diagnosis of SAD; intervention: fluvoxamine; study design: placebo-controlled randomized controlled trials (RCTs); outcomes: efficacy and tolerability outcomes. METHODS: We conducted a comprehensive search of PubMed, Embase, Cochrane Central Register of Controlled Trials, Web of Science, and ClinicalTrials.gov for RCTs on January 3, 2018. Review Manager 5.3 and Stata Version 12.0 software were used for all statistical analyses. Mean differences (MDs) with 95% confidence intervals (CIs) were calculated for continuous variables, and odds ratios (ORs) with 95% CIs were calculated for dichotomous variables. Cochrane Collaboration's risk of bias tool was used to assess the likelihood of risk of bias. Efficacy was assessed by mean changes in the Liebowitz Social Anxiety scale (LSAS) total score and the Clinical Global Impression Severity of Illness (CGI-S) score as well as the response rate. Tolerability was mainly assessed by the discontinuation rate due to adverse events (AEs) and the incidence of most frequent treatment-emergent AEs (TEAEs). RESULTS: This meta-analysis included 5 RCTs. Mean changes in LSAS total and CGI-S scores were both significantly greater in patients treated with fluvoxamine than those treated with placebo (LSAS: MD = 11.90, 95% CI = 8.09-15.71, P < .001; CGI-S: MD = 0.52, 95% CI = 0.33-0.72, P < .001). Response rate was higher in fluvoxamine group as compared with placebo (OR = 1.71, 95% CI = 1.30-2.24, P < .001). Additionally, mean change in the Sheehan disability scale score was significantly greater in fluvoxamine group than placebo group (OR = 2.11, 95% CI = 1.03-3.18, P < .001). The discontinuation rate due to AEs was higher in patients that received fluvoxamine compared to those received placebo (OR = 5.99, 95% CI = 2.24-15.99, P < .001), as was the incidence of overall TEAEs (any AE) (OR = 2.66, 95% CI = 1.77-4.02, P < .001). However, the incidence of serious AEs was not significantly different between the 2 groups (OR = 0.99, 95% CI = 0.25-3.89, P = .99). CONCLUSION: Fluvoxamine was found to be effective in adult patients with SAD, with acceptable tolerability.

Vitamin D and DDX4 regulate the proliferation and invasion of ovarian cancer cells.

Ovarian cancer is one of the most commonly occurring types of cancer and one of the most common causes of cancer-associated mortality in women. Diagnosis of ovarian cancer at an early stage is difficult due to the lack of specific symptoms. In the present study, it is demonstrated that active vitamin D treatment prohibited the proliferation and invasion of ovarian cancer cells, and the expression level of a germ cell specific marker DEAD (Asp-Glu-Ala-Asp)-box helicase 4 (DDX4), which is overexpressed in ovarian cancer, was downregulated by active vitamin D treatment. Knockdown of DDX4 by siRNA could also suppress the invasive ability of ovarian cancer cells. Therefore, DDX4 may be considered as a diagnostic marker of ovarian cancer, and vitamin D may be a candidate drug for ovarian cancer therapy.

Long non-coding RNA PVT1 promotes cell proliferation and invasion through regulating miR-133a in ovarian cancer.

The long non-coding RNA, plasmacytoma variant translocation 1 (PVT1), was reportedly to be highly expressed in a variety of tumors including ovarian cancer (OC). However, the role and mechanism of action of PVT1 in the carcinogenesis and progression of OC remains largely unknown. PVT1 and miR-133a expression were detected by quantitative real time PCR(qRT-PCR) assays in OC tissues and cell lines. Cell Counting Kit-8 (CCK-8), flow cytometer, wound healing and transwell invasion assays were performed to evaluate cell proliferation, cycle, migration and invasion abilities, respectively. qRT-PCR and luciferase reporter assays demonstrated PVT1 regulated miR-133a expression. Here, we discovered that PVT1 shows higher expression in OC tissues than in normal ovarian tissues, and patients who show higher expression of PVT1 have worse progression-free and overall survivals compared to lower expression of PVT1. Additionally, we observed that knockdown of PVT1 significantly inhibited OC cell proliferation, and decreased the migration and invasion capabilities of OC cells. Mechanistically, miR-133a was identified to serve as a direct downstream target of PVT1 in OC. Knockdown of PVT1 inhibited cell proliferation, migration and invasion through negative regulating miR-133a in OC cells. Taken together, our finding shows that PVT1 may be a novel biomarker for prognosis and a promising therapeutic target for OC.

MiR-548c impairs migration and invasion of endometrial and ovarian cancer cells via downregulation of Twist.

BACKGROUND: MicroRNAs (miRNAs) are a class of small non-coding RNAs, which post-transcriptionally repress the expression of genes involved in cancer initiation and progression. Although some miRNAs that target many signaling pathways (also called universe miRNAs) are supposed to play a global role in diverse human tumors, their regulatory functions in gynecological cancers remain largely unknown. We investigated the biological role and underlying mechanism of miR-548c (one universe miRNA) in endometrial and ovarian cancer. METHODS: The effects of miR-548c overexpression on cell proliferation, migration and invasion were studied in endometrial and ovarian cancer cells. TWIST1 (Twist) was identified as a direct miR-548c target by western blot analysis and luciferase activity assay. The expression of miR-548c and Twist were examined by qRT-PCR in endometrial and ovarian cancer tissues. RESULTS: Here, we report that miR-548c is down-regulated in endometrial and ovarian cancer tissues when compared to normal tissues, and our meta-analysis reveal that decreased miR-548c expression correlates with poor prognosis in endometrial cancer patients. We show that in endometrial and ovarian cancer cells, ectopic expression of miR-548c significantly inhibits whereas knockdown of miR-548c dramatically induces cancer cell proliferation, migration and invasion. By using luciferase reporter assay, we demonstrate that Twist, a known oncogene in endometrial and ovarian cancers, is a direct target of miR-548c. Furthermore, the expression of Twist partially abrogates the tumor suppressive effects of miR-548c on cell migration and invasion. CONCLUSION: These findings suggest that miR-548c directly downregulates Twist, and provide a novel mechanism for Twist upregulation in both endometrial and ovarian cancers. The use of miR-548c may hold therapeutic potential for the treatment of Twist-overexpressing tumors.