Endometrial cancer (EC) incidence is rising globally, yet diagnosis still depends on invasive procedures, which limit accessibility and delay early detection. A noninvasive, accurate, and accessible diagnostic assay is urgently needed to enable early EC detection. In this multicenter diagnostic study across six hospitals in China (May 2021 - May 2026), we integrated whole-epigenome methylation profiling of 1,211 datasets followed by targeted bisulfite sequencing of 367 samples to identify EC-specific urine DNA methylation biomarkers. A qPCR-based urinary methylation assay (Urine-qEC) targeting three genes, VWC2, ZNF132, and ZSCAN12, was subsequently developed and validated in a cross-sectional multicenter cohort (n = 587). Urine hypermethylation signatures exhibited concordance with EC tumors and significantly diminished after tumor resection. The Urine-qEC assay achieved an AUC of 0.976 (89.4

Purpose:To construct a new clinical staging system including the number of lymph node metastases to supplement the International Federation of Gynecology and Obstetrics (FIGO) staging for the prognosis of endometrial carcinoma patients. Methods:This cohort study retrieved the data of 28,824 patients confirmed as endometrial carcinoma between 2010 and 2015 in the surveillance, epidemiology, and end results (SEER) database. COX risk proportional model was established to evaluate the association between FIGO staging with the all-cause mortality of endometrial carcinoma. The diagnostic value of FIGO staging and the new staging for the mortality of patients were evaluated by receiver operator characteristic curve (ROC). Hazard ratio (HR) and 95% confidence interval (CI) were effect size. Results:The 5-year survival rate of all participants was 77.21%. The median follow-up time was 60.00 (60.00,60.00) months. Patients at FIGO staging IB (HR=1.75, 95% CI: 1.62-1.90), FIGO staging II (HR=2.22, 95% CI: 2.00-2.47), FIGO staging IIIA (HR=2.74, 95% CI: 2.43-3.09), FIGO staging IIIB (HR=4.07, 95% CI: 3.48-4.76), FIGO staging IIIC1 (HR=3.84, 95% CI: 3.52-4.20), FIGO staging IIIC2 (HR=4.52, 95% CI: 4.09-4.99), FIGO staging IVA (HR=5.56, 95% CI: 4.58-6.74), and FIGO staging IVB (HR=7.62, 95% CI: 6.94-8.36) were associated with increased risk of all-cause mortality of endometrial carcinoma patients. After adding positive lymph nodes as another covariate in Model 3, the effect on of FIGO staging survival was reduced when the FIGO staging was higher than stage III/IV. The C-index of the new staging 0.781 (95% CI: 0.774-0.787) was higher than FIGO staging 0.776 (95% CI: 0.770-0.783). Conclusion:Our new staging using the number of positive lymph nodes supplement to the FIGO staging was superior than the FIGO staging for predicting the prognosis of endometrial cancer patients, which might help more accurately identify endometrial carcinoma patients who were at high risk of mortality and offer timely treatments in these patients.

Abstract Background The glioblastoma-amplified sequence (GBAS) is a newly identified gene that is amplified in approximately 40% of glioblastomas. This article probes into the expression, prognostic significance, and possible pathways of GBAS in ovarian cancer (OC). Method Immunohistochemical methods were used to evaluate the expression level of GBAS in OC and its relationship with clinicopathological characteristics and prognosis. Glioblastoma-amplified sequence shRNA was designed to transfect into OC cell lines to silence GBAS expression, then detect the proliferation, apoptosis, and migration ability of the cell. Furthermore, an in vitro tumor formation experiment in mice was constructed to prove the effect of GBAS expression on the growth of OC in vivo. To further study the regulation mechanism of GBAS, we performed co-immunoprecipitation (Co-IP) and shotgun LC-MS mass spectrometry identification. Results Immunohistochemistry indicated that GBAS was markedly overexpressed in OC compared with normal ovarian tissue and was associated with lymph node metastasis. Inhibition of GBAS expression can significantly reduce OC cell proliferation, colony formation, promote cell apoptosis, and reduce the ability of cell migration and invasion. In vivo tumor formation experiments showed that the size and weight of tumors in mice after GBAS expression knockdown was significantly smaller. Glioblastoma-amplified sequence may be combined with elongation factor 1 alpha 1 (eEF1A1) to achieve its regulation in OC. Bioinformatics analysis data indicate that GBAS may be a key regulator of mitochondria-associated pathways, therefore controlling cancer progression. MicroRNA-27b, MicroRNA-23a, and MicroRNA-590 may directly targeting GBAS affects the biological behavior of OC cells. Conclusion The glioblastoma-amplified sequence may regulate the proliferation and metastasis of OC cells by combining with eEF1A1.

Ellagic acid has been reported to possess various activities, including anti-inflammatory, anti-oxidative, antiviral and anticancer abilities. However, the effect and underlying molecular mechanism of ellagic acid on cervical carcinoma remain unclear. Therefore, the present study aimed to investigate the effects of ellagic acid on human cervical carcinoma cells and the molecular mechanism involved. The present study assessed the survival of HeLa cells cultured in vitro using an MTT assay. Apoptosis rate and cell cycle of HaLa cells were measured using an Annexin V-Fluorescein isothiocyanate/propidium iodide Apoptosis Detection and Cell Cycle Analysis kits, respectively, following treatment with varying concentrations of ellagic acid. Further effects of ellagic acid on HeLa cells was assessed using flow cytometry and western blotting. Ellagic acid treatment significantly inhibited cell proliferation of the human cervical carcinoma HeLa, SiHa and C33A cells. In HeLa cells, it was observed that ellagic acid arrested the cell cycle at G1 phase, induced cell apoptosis, suppressed the phosphorylation of Janus kinase 2 and signal transducer and activator of transcription 3 (STAT3), as well as modulated the expression of associated proteins. Collectively, the results of the present study provide evidence that ellagic acid inhibits cervical carcinoma cell proliferation, and induces apoptosis and cell cycle arrest at G1 phase possibly via the regulation of STAT3 signaling.

Background/Aims: Ovarian cancer (OC) causes more death and serious conditions than any other female reproductive cancers, and many expression signatures have been identified for OC prognoses. However, no significant overlap is found among signatures from different studies, indicating the necessity of signature identifications at the functional level. Methods: We performed an integrated analyses of miRNA and gene expressions to identify OC prognostic subpathways (pathway regions). Using The Cancer Genome Atlas data set, we identified core prognostic subpathways, and calculated subpathway risk scores using both miRNA and gene components. Finally, we performed global risk impact analyses to optimize core subpathways using the random walk algorithm. Results: Subpathway-level analyses displayed more robust results than the gene- and miRNA-level analyses. Moreover, we verified the advantage of core subpathways over the entire pathway-based results and their prognostic performance in two independent validation data sets. Based on the global impact score, 13 subpathway signatures were selected and a combined subpathway-based risk score was further calculated for OC patient prognoses. Conclusions: Overall, it was possible to systematically perform integrated analyses of the expression levels of miRNAs and genes to identify prognostic subpathways and infer subpathway risk scores for use in OC clinical applications.

This study was intended to analyze effects of lncRNA CRNDE on cervical cancer cell growth and metastasis. Fifty pairs of cervical cancer tissues and corresponding adjacent tissues were collected. Expressions of long non-coding RNAs (lncRNAs) in tissue samples were detected by microarray analysis. Expression levels of CRNDE in cervical cancer cells and normal cells were detected by qRT-PCR. Cell-counting kit-8 (CCK-8) assay and clone formation assay were utilized to evaluate cell growth. Wound healing assay and Transwell assay were conducted to detect the migratory and invasive capability of cervical cancer cells. The expressions of CRNDE in cervical cancer tissues and cells were higher than those in normal tissues and cells. CCK-8 assay and clone formation assay showed that the knockdown of CRNDE could inhibit the cell proliferation of HeLa and C-33A cells. Wound healing assay indicated that the downregulation of CRNDE expression could suppress the cell migration. The result of a Transwell assay demonstrated that the number of invasion cells reduced in the CRNDE-si group in comparison with the Mock group. LncRNA CRNDE could promote the cell growth and stimulate the metastasis of cervical cancer cells.

MicroRNAs (miRNAs) participate in post-transcriptional regulation by targeting the 3' untranslated region of target genes that are involved in diverse biological processes. To the best of our knowledge, the association between miR-152 and ERBB3 in ovarian cancer remains unclear. In the present study, a negative correlation between miR-152 and ERBB3 in ovarian cancer was observed. The luciferase reporter gene assay results demonstrated that miR-152 negatively regulated ERBB3 in SKOV3 and OVCAR3 ovarian cancer cells. Furthermore, our results revealed that miR-152 suppressed the ability of ovarian cancer cell proliferation, migration and invasion, and promoted apoptosis through inhibiting ERBB3 in vitro. Therefore, in the present study, miR-152 was found to be involved in the proliferation and metastasis of ovarian cancer cells through repression of ERBB3 expression. Therefore, miR-152 may be a potential therapeutic target for the treatment of ovarian cancer.

The nucleocapsid (N) protein is the most conserved structural protein in equine arteritis virus (EAV). This study aimed to identify the minimal conserved B cell epitope on the EAV N protein. The purified N protein was used to immunize mice for preparing monoclonal antibody (mAb). The reactivity of mAb was evaluated by Western blot and immunofluorescence assay. Moreover, 11 overlapping peptides (named MBP-N1 to MBP-N11) were designed to localize the linear antigenic epitope within the N protein. The peptides were identified by indirect enzyme-linked immunosorbent assay (ELISA) and Western blot. The minimal conserved B cell epitope on the EAV N protein was identified. The homology analysis was also performed. An EAV N-reactive mAb was selected and designated as 1C11. Indirect ELISA results showed that overlapping domain between MBP-N10 and MBP-N11 was recognized by the mAb 1C11. Furthermore, the indirect ELISA and Western blot showed that (101)QRKVAP(106) was the minimal linear epitope of the EAV N protein. The homology analysis showed that the identified epitope was conserved among all EAV strains analyzed in this work, with the exception of the ARVAC. One EAV N-specific mAb (1C11) was developed, and a minimal linear peptide epitope ((101)QRKVAP(106)) within the N protein was identified.