European journal of gynaecological oncology最新文献

{"title":"Curcumin enhances breast cancer cell death by suppressing PD-L1 expression","authors":"","doi":"10.22514/ejgo.2025.066","DOIUrl":"https://doi.org/10.22514/ejgo.2025.066","url":null,"abstract":"Background: To investigate the effects of curcumin on the growth of breast cancer (BC) cells in vitro and to explore the role of Programmed death ligand 1 (PD-L1) in this process. Methods: Curcumin’s effects on the growth and apoptosis of MCF-7 and MDA-MB-231 breast cancer cells were assessed using cell counting kit-8 (CCK-8), flow cytometry and Western blotting. The inhibition of PD-L1 expression by curcumin was evaluated through co-transfection of PGL3-PD-L1 plasmids and luciferase activity. Additionally, the Phosphatidylinositol 3-Kinase (PI3K)/Protein Kinase B (AKT)/mechanistic target of rapamycin (mTOR) pathway was analyzed after treatment with curcumin and the PD-L1 inhibitor BMS202. Results: Curcumin had anti-proliferative and pro-apoptosis effects on human breast cancer cells. Curcumin significantly inhibited the expression level of both the PD-L1 protein and the PD-L1 mRNA in BC cells. The abundance of PD-L1 transcripts in the BC cells with curcumin decreased significantly, but increased with the increase in curcumin concentration. The activity of luciferase significantly decreased with the increase in concentration of the breast cancer cells transfected with PD-L1 promoter after treatment with curcumin. Curcumin also induced the inhibition of PD-L1 expression, and mediates the inhibition of the PI3K/AKT/mTOR axis. Conclusions: The combination of curcumin and PD-L1 inhibits the proliferation of BC cells and induces apoptosis, which may be related to curcumin’s inhibition of the activity of PD-L1 promoter and the downstream PI3K/AKT/mTOR axis.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"46 5","pages":"60-60"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147910124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxycodone modulates VEGFA to inhibit cervical cancer cell migration and angiogenesis","authors":"","doi":"10.22514/ejgo.2025.053","DOIUrl":"https://doi.org/10.22514/ejgo.2025.053","url":null,"abstract":"Background: Cervical cancer (CC) is a leading cause of cancer-related deaths among women worldwide, necessitating the development of novel therapeutic strategies. Oxycodone, a semi-synthetic opioid, is primarily known for its analgesic properties but has shown potential anti-cancer effects in various malignancies. However, its impact on cervical cancer cells and the underlying mechanisms remain unclear. Methods: Human cervical cancer cell lines Hela and Siha were treated with varying concentrations of oxycodone (10, 20, 40 μg/mL). Cell proliferation was assessed using Cell Counting Kit-8 (CCK-8) and clonogenic assays. Apoptosis was measured by flow cytometry. Cell migration and angiogenesis were evaluated using wound healing and tube formation assays, respectively. VEGFA expression was analyzed by Western blotting. Results: Oxycodone inhibited the proliferation of cervical cancer cells. It induced apoptosis in cervical cancer cells. Oxycodone suppressed the migration and angiogenesis of cervical cancer cells. Mechanistically, oxycodone regulated vascular endothelial growth factor A (VEGFA) expression, leading to the inhibition of cell migration and angiogenesis. Conclusions: Oxycodone exhibits significant anti-cancer effects on cervical cancer cells by inhibiting proliferation, inducing apoptosis, and suppressing migration and angiogenesis through the regulation of VEGFA expression. These findings suggest that oxycodone has potential as a therapeutic agent for cervical cancer treatment.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"46 4","pages":"73-73"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147920929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and validation of a novel gene signatures based on a random forest algorithm and artificial neural network for predictive diagnosis of cervical squamous cell carcinoma","authors":"","doi":"10.22514/ejgo.2025.034","DOIUrl":"https://doi.org/10.22514/ejgo.2025.034","url":null,"abstract":"Background: Effective treatment of cervical carcinoma can be challenging due to the lack of specific symptoms in the initial phase, as well as patients often only seeking medical attention in the middle and late stages of the disease when symptoms become more apparent. This study aims to address these limitations by developing and validating a gene signature for predicting cervical squamous cell carcinoma (CESC) using both the random forest algorithm and artificial neural network. Methods: Potential predictive genes for CESC were identified by analyzing three matrix datasets containing tissues from individuals with normal cervical epithelium and patients with CESC. Then, the random forest algorithm and artificial neural network were used to construct predictive models for CESC diagnosis, which were validated using both an independent validation dataset and in vitro experiments. To confirm the validity of the identified genes, protein and mRNA expression of eight disease signature genes were detected in the two groups using Western blotting and real-time quantitative polymerase chain reaction. Additionally, immunoinfiltration analysis was performed. Results: A total of 241 differentially expressed genes (DEGs) were identified, based on which eight genes with the highest predictive ability were selected and used to construct a molecular prognostic scoring system, which demonstrated exceptional predictive accuracy (Area Under Curve (AUC) = 0.995). Validation using an independent dataset confirmed the model’s remarkable predictive ability (AUC = 1.000). In vitro experiments demonstrated significant differences in the expression of the eight disease signature genes between the two groups. Immunoinfiltration analysis also revealed significant differences in immune cell infiltration, with squamous cell carcinoma of the cervix showing a higher degree of macrophage infiltration than normal cervical epithelium. Conclusions: Random forest algorithm and artificial neural network were used to obtain new gene signatures, based on which a molecular prognostic scoring system was developed to predict CESC and aid clinical decision-making.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"46 3","pages":"34-34"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147903676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phillyrin restrains breast cancer cell growth by inducing ferroptosis","authors":"","doi":"10.22514/ejgo.2025.132","DOIUrl":"https://doi.org/10.22514/ejgo.2025.132","url":null,"abstract":"Background: Breast cancer is one of the most common malignant tumors worldwide, predominantly affecting women and associated with high mortality. Phillyrin (PHN), a bioactive compound isolated from Forsythia suspensa (Thunb.) Vahl has been confirmed to possess diverse biological activities, including anti-inflammatory, antioxidant, and anti-tumor effects. Nevertheless, its regulatory role in breast cancer progression remains unclear. Methods: Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay, while proliferative capacity was evaluated through colony formation assay. Apoptosis was determined by flow cytometry. The level of reactive oxygen species (ROS) was measured by 2′,7′-dichlorofluorescein diacetate (DCFH-DA) staining. The concentrations of malondialdehyde (MDA), glutathione (GSH), and Fe2+ were quantified using the corresponding detection kits. Protein expression levels were analyzed by western blotting. Results: PHN significantly inhibited breast cancer cell growth and induced ferroptosis. Treatment with 50 µmol/L PHN reduced cell proliferation, an effect that was reversed by Ferrostatin-1 (Fer-1), a ferroptosis inhibitor. Furthermore, PHN was shown to suppress activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. Conclusions: PHN inhibited breast cancer cell growth by inducing ferroptosis and suppressing the PI3K/Akt pathway. These findings suggest that PHN may represent a potential therapeutic agent for the treatment of breast cancer.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"46 10","pages":"59-59"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147909874","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of TSPAN1 inhibits angiogenesis in triple-negative breast cancer cells by regulating the PI3K/Akt signaling pathway","authors":"","doi":"10.22514/ejgo.2025.122","DOIUrl":"https://doi.org/10.22514/ejgo.2025.122","url":null,"abstract":"Background: Triple-negative breast cancer (TNBC) progression and invasion highly depends on abnormal angiogenesis. While tetraspanin 1 (TSPAN1) has been implicated in the malignant progression of TNBC, its relationship in tumor angiogenesis remains poorly understood. Methods: Tumor samples were collected from patients with TNBC and analyzed using clinical pathological and Western blot analyses. TSPAN1 expression was knocked down in the TNBC cell line, Hs-578T using siRNA technology. The angiogenic ability of human umbilical vein endothelial cells (HUVECs) was evaluated by lumen formation assay. The Phosphatidylinositol 3-Kinase (PI3K)/Protein Kinase B (Akt) signaling pathway was detected using western blots. Results: TSPAN1 overexpression in TNBC tumors is linked to metastasis and PI3K/Akt pathway activation. Knockdown of TSPAN1 in TNBC cells, significantly suppressed the tube formation ability of co-cultured HUVECs. Mechanistically, TSPAN1 knockdown significantly inhibited the activity of the PI3K/Akt pathway. Conclusions: In conclusion, TSPAN1 promotes TNBC angiogenesis via activation of PI3K/Akt signaling pathway.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"46 9","pages":"71-71"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147890791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KRT15 promotes proliferation, migration and invasion of cervical cancer cells","authors":"","doi":"10.22514/ejgo.2025.086","DOIUrl":"https://doi.org/10.22514/ejgo.2025.086","url":null,"abstract":"","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"46 6","pages":"121-121"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147918579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of NEIL3 inhibits the growth of breast cancer cells by mediating the PI3K/Akt/mTOR axis","authors":"","doi":"10.22514/ejgo.2025.042","DOIUrl":"https://doi.org/10.22514/ejgo.2025.042","url":null,"abstract":"Background: To explore the role of Nei endonuclease VIII-like 3 (NEIL3) in breast cancer (BC) cell proliferation and motility and its underlying mechanism. Methods: BC cell lines were analyzed. NEIL3 expression levels in BC tissues was assessed using the UALCAN and Kaplan-Meier Plotter databases. NEIL3 knockdown was performed using siRNAs, and its effects on cell growth, motility, Epithelial-Mesenchymal Transition (EMT) markers, and the Phosphoinositide 3-Kinase/Protein Kinase B/Mammalian Target of Rapamycin (PI3K/Akt/mTOR) axis were evaluated using Immunoblotting, cell counting kit-8 (CCK-8) assays, colony formation, Transwell as well as wound healing assays. Results: NEIL3 was highly expressed in BC tissues and cell lines. NEIL3 knockdown inhibited cell growth, motility and reduced EMT marker expression. It also decreased phosphorylation levels of proteins, indicating inhibition of the PI3K/Akt/mTOR axis. Conclusions: NEIL3 mediates BC cell proliferation as well as motility by activating the PI3K/Akt/mTOR axis. Targeting NEIL3 may offer a new approach to combat BC.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"46 3","pages":"105-105"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147907266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of PHLDA2 promotes apoptosis and autophagy in endometrial cancer cells while inhibiting their proliferation and metastasis","authors":"","doi":"10.22514/ejgo.2025.071","DOIUrl":"https://doi.org/10.22514/ejgo.2025.071","url":null,"abstract":"Background: Pleckstrin homology-like domain family A member 2 (PHLDA2) has been implicated as a potential inhibitor of apoptosis and may contribute to tumorigenesis. Here, we report on the function of PHLDA2 in endometrial cancer (EC). Methods: Small interfering RNA (siRNA) was utilized to reduce PHLDA2 expression in EC cells. Subsequently, cell proliferation, apoptosis, migration and invasion abilities were evaluated. Autophagy was examined through Microtubule-associated protein 1 light chain 3 beta (LC3B) immunofluorescence staining. Protein expression levels were determined by Western blotting. Results: PHLDA2 expression was significantly elevated in EC cell lines, and its knockdown was found to reduce cell proliferation, migration, and invasion while enhancing apoptosis. Moreover, induction of autophagy was observed with PHLDA2 knockdown, marked by elevated LC3B conversion and diminished P62 expression. Additionally, the fall in phosphorylation levels of Phosphatidylinositol 3-kinase (PI3K), Protein kinase B (AKT) and Glycogen synthase kinase-3 beta (GSK-3β) was examined following PHLDA2 knockdown. Conclusions: PHLDA2 knockdown can impede the malignant progression of EC cells by promoting apoptosis and autophagy, potentially through inactivation of the PI3K/AKT/GSK-3β pathway.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"46 5","pages":"107-107"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147907817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FKBP10 ablation promotes breast cancer chemosensitivity via targeting autophagy and the AKT/CREB axis","authors":"","doi":"10.22514/ejgo.2025.138","DOIUrl":"https://doi.org/10.22514/ejgo.2025.138","url":null,"abstract":"","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"46 11","pages":"60-60"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147881871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of PIMREG modulates the Wnt/β-catenin pathway to suppress proliferation and stemness in endometrial cancer","authors":"","doi":"10.22514/ejgo.2025.099","DOIUrl":"https://doi.org/10.22514/ejgo.2025.099","url":null,"abstract":"Background: Endometrial cancer is the most common gynecological malignancy, and poses serious threat to health. PIMREG (PICALM interacting mitotic regulator also known as FAM64A), has been uncovered in promoting tumorigenesis in multiple cancers. But, its regulatory impacts in endometrial cancer remain poorly understood. Methods: Cell viability was assessed by the Cell Counting Kit-8 (CCK-8) assay. Protein levels were inspected by Western blotting. Cell proliferation was evaluated by colony formation assay, while stemness was examined by sphere formation assays. Results: PIMREG expression was found to be upregulated in endometrial cancer. Suppression of PIMREG significantly reduced cell viability and suppressed proliferative and stemness capacities. Furthermore, silencing PIMREG retarded the evoking of the Wnt/β-catenin signaling pathway. Conclusions: PIMREG knockdown suppressed proliferation and stemness by modulating the Wnt/β-catenin pathway in endometrial cancer. This project hinted that PIMREG may be one useful therapeutic target for endometrial cancer treatment.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"46 7","pages":"88-88"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147890938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}