European journal of gynaecological oncology最新文献

{"title":"Knockdown of GDF15 inhibits endometrial cancer cell proliferation and EMT","authors":"","doi":"10.22514/ejgo.2024.053","DOIUrl":"https://doi.org/10.22514/ejgo.2024.053","url":null,"abstract":"Endometrial cancer (EC) is a malignant tumor affecting the uterine upper layer. Despite recent advancements, identifying new therapeutic targets remains important for improving patient prognosis. Growth differentiation factor 15 (GDF15) belongs to the Transforming Growth Factor (TGF)-β superfamily and is often upregulated in pathological conditions, including injury and cancers. However, its involvement in EC remains poorly understood. This study aims to elucidate the significance of GDF15 in EC and its potential underlying mechanism. Our results indicate increased GDF15 expression levels in EC tissues, and the knockdown of GDF15 was found to suppress EC cell growth and epithelial-mesenchymal transition (EMT). Moreover, GDF15 depletion inhibited the TGF-β pathway activation. In summary, GDF15 can promote EC cell growth and EMT by modulating the TGF-β/Smad2/Smad3 axis.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 3","pages":"95-95"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147883397","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":"Apigenin inhibits the proliferation and aerobic glycolysis of endometrial cancer cells by regulating the PI3K/Akt signaling pathway","authors":"","doi":"10.22514/ejgo.2024.100","DOIUrl":"https://doi.org/10.22514/ejgo.2024.100","url":null,"abstract":"This study investigated the effects of apigenin on endometrial cancer cell proliferation, apoptosis and aerobic glycolysis. The cell viability and cell proliferation of endometrial cancer cells were detected using Cell Counting Kit-8 (CCK8) kit and5-ethynyl-2′-deoxyuridine (EDU) staining. Flow cytometry analysis was used to detect the rate of apoptosis in endometrial cancer cells. Lactate production, glucose consumption, and Adenosine triphosphate (ATP) levels were also measured. Western blot was used to detect the expression of Bcl2-Associated X (BAX), B-cell lymphoma 2 (BCL-2), Cleaved Caspase-3, phosphoinositide 3-kinase (PI3K), p-PI3K, rapamycin (mTOR), p-mTOR, Phosphatase and tensin homolog (PTEN), protein kinase B (Akt) and p-Akt. The results showed that, apigenin inhibits cell viability, cell proliferation, promotes the rate of apoptosis, and the expression of BAX, Cleaved Caspase-3, and inhibits the expression of BCL-2 of endometrial cancer cells in a dose-dependent manner. In addition, apigenin suppressed lactate production, glucose consumption, and ATP levels and inhibited the phosphorylation of PI3K and Akt in a dose-dependent manner. Finally, apigenin inhibited the proliferation and aerobic glycolysis of endometrial cancer cells and promoted cell apoptosis by blocking the PI3K/Akt signaling pathway.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 5","pages":"125-125"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147907539","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":"Anticancer potential of Marsdenia tenacissima extract: modulation of proliferation, apoptosis and SBEM gene expression in triple-negative breast cancer MDA-MB-231 cells","authors":"","doi":"10.22514/ejgo.2024.115","DOIUrl":"https://doi.org/10.22514/ejgo.2024.115","url":null,"abstract":"Marsdenia tenacissima (MT) is a herbal remedy that has been used for many years to treat cancer. While the anti-cancer properties of Marsdenia tenacissima extract (MTE) have been observed in several malignancies, its effect on the fundamental mechanisms of triple-negative breast cancer cells remains unclear. Here, we investigate the underlying anti-cancer mechanisms of MTE in MDA-MB-231 cells in regard to their proliferation, apoptosis, and the expression of the secretory breast epithelial mucin (SBEM) gene. Cell Counting Kit-8 (CCK-8) and Annexin V and propridium iodide (PI) staining kits were used to measure the proliferation and apoptosis in MDA-MB-231 cells, respectively. The effects of MTE on MDA-MB-231 cell migration were evaluated via scratch healing at 0 and 24 hours after treatment with different MTE concentrations. Western blot was used to detect the protein expressions of SBEM and apoptosis-related factors. Real-time quantitative Polymerase Chain Reaction (RT-qPCR) was performed to detect SBEM mRNA expression after different drug concentrations. CCK-8 assays indicated increased proliferation and inhibition of MDA-MB-231 cells with increasing MTE concentrations. Flow cytometry also showed a gradual dose-dependent increase in MDA-MB-231 cell apoptosis rate with increasing MTE concentrations. Additionally, MTE reduced the migration of MDA-MB-231 cells in a dose-dependent way. Proteomic experiments showed that the drug group downregulated the expression levels of B-cell Lymphoma-2 (BCL-2), B-cell lymphoma-extra large (BCL-XL) and SBEM in MDA-MB-231 cells, and RT-qPCR analysis showed that the expression of SBEM mRNA in MDA-MB-231 cells could be down-regulated in a dose-dependent manner by MTE. MTE exerted its anti-cancer effects on MDA-MB-231 cells by inhibiting their proliferation and migration, as well as inducing cell apoptosis. These effects might be associated with the down-regulation of BCL-2 and BCL-XL expression and the deregulation of SBEM mRNA expression.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 6","pages":"40-40"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147906145","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":"CENPU affects the paclitaxel resistance of cervical cancer cells by regulating the FOXM1/ABCC5 pathway","authors":"Xia Zhang, Yuanyi Zhang, Min Wang, S Pimple, G Mishra, F Ito, H Nomura, M Ito, K Takahashi, T Fujii, S Hayashi, T Kasamatsu, T Arimoto, Yi Xiongh, J Hu, H Zeng, L Liu, H Zhou, J Sharifi-Rad, C Quispe, J Patra, Y Singh, M Panda, G Das, X Long, M Zheng, Y Yang, Y Chen, X Zhang, H Zhang, A Modi, P Purohit, D Roy, J Vishnoi, P Pareek, P Elhence, D Zhou, J Liu, F Liu, G Luo, H Li, R Zhang, Y Hou, Z Dong, W Zhong, L Yin, X Li, G Kuerban, F Kashgari, A Ravna, G Sager, R Lysa, I Enyedy, E Dietrichs, Y Zhang, W Zhang, L Sun, Y Yue, D Shen, B Tian, S Zhao, Y Geng, L Cao, Q Yang, T Pan, D Zhou, Q Zhang, Y Li, S Zhang, Y Shi, Y Yu, X Chen, W Zhang, J Liu, X Wang, D Chen, J Gao, H Long, H Zha, A Zhang, Y Qu, L Song, S Xu, Msy Yu, O Kadioglu, F Michelangeli, Y Zhu, F Yu, Y Jiao, J Feng, W Tang, H Yao, X Zhang, M Wang, Y Zhang, J Yang, W Duan, Y Liu, Y Yao, B Liao, H Zhang, Z Yang, P Xia, T Deng, X Jiang, Z He, M Cai, C Chen, Z Xu","doi":"10.22514/ejgo.2024.014","DOIUrl":"https://doi.org/10.22514/ejgo.2024.014","url":null,"abstract":"In cervical cancer (CC), the efficacy of chemotherapy is often hindered by the development of paclitaxel (PTX) resistance, even in patients who initially responded to chemotherapy. However, the mechanisms underlying PTX resistance in CC patients remain unclear. In this study, we uncover a unique role played by CENPU (centromeric protein U, also known as PBIP1/KLIP1/CENP-50/MLF1IP) in association with paclitaxel resistance in CC cells. First, we established paclitaxel-resistant cell lines from Hela and SiHa cells (designated as Hela/PTX and SiHa/PTX) and confirmed their resistance by determining the half-maximal inhibitory concentration (IC50) values and assessing cell viability. The results demonstrated that Hela/PTX and SiHa/PTX cells exhibited an elevated IC50 and enhanced cell proliferation, accompanied by a decrease in apoptosis. Subsequently, si-CENPU was used to silence CENPU in Hela/PTX and SiHa/PTX cells, which led to a reduction in cell viability and an increase in cell apoptosis, indicating that the silencing of CENPU mitigated paclitaxel resistance in Hela/PTX and SiHa/PTX cells. Furthermore, CENPU knockdown suppressed Forkhead box M1 (FOXM1) and Adenosine Triphosphate (ATP) binding cassette subfamily C member 5 (ABCC5) expression in Hela/PTX and SiHa/PTX cells. Interestingly, the alleviating effects of CENPU silencing on paclitaxel resistance in CC cells were compromised when FOXM1 levels were supplemented, indicating that CENPU knockdown could attenuate PTX resistance by downregulating the FOXM1/ABCC5 signaling pathway. In conclusion, our study reveals an elevated expression of CENPU in paclitaxel-resistant CC (Hela/PTX and SiHa/PTX) and demonstrates that the knockdown of CENPU can mitigate paclitaxel resistance in CC cells by deregulating the FOXM1/ABCC5 signaling pathway.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 1","pages":"89-89"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://oss.ejgo.net/files/article/20240206-279/pdf/EJGO2023082401.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147911578","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":"Taraxasterol stimulates apoptosis of BCa cells via restraining PI3K/AKT and epidermal growth factor receptor (EGFR)","authors":"Yanjun Hu, Xiping Zhang, Shuai Zhao, Y Wang, C Zhang, L Mai, Y Niu, Y Wang, Y Bu, A Patra, S Satpathy, M Hussain, S Krmer, C Rogmans, D Saylan, D Friedrich, C Kraft, G Rogmans, M Bordignon, Pesce Viglietti, A Julia, E Sanchez, M Rolle, A Mando, P, K Lin, C Lengacher, C Rodriguez, L Szalacha, J Wolgemuth, C Tang, J Yang, Z Liu, Y Chen, C Zeng, R Sang, B Ge, H Li, H Zhou, K Yan, W Wang, F Ren, Y Zhang, Y Qin, J Shang, Y Wang, P Wei, J Lu, B Shuai, Z Shou, W Guo, C Zhou, X Ouyang, B Ge, R Sang, Wang Yan, K Yu, Y Kong, L, G Li, D Zhang, S Wang, N Jie, Y Qin, C Li, M Wang, X Chen, Chen, J Yin, Y Lin, W Fang, X Zhang, J Wei, G Hu, O Karginova, C Weekley, Raoul Alsayed, A Wu, T Lee, S, Y Pan, Q Zhang, H Zhang, F Kong, Y Luan, K Ren, Y Luan, X Chen, Y Yang, Y Luan, Y Luan, R Yuan, Q Feng, X Chen, Y Yang, X Ye, R Xu, S Liu, B Hu, Z Shi, F Shi, J Wang, K Zheng, Y Jin, Y Fu, R Wang, J Zhang, W Liu, Q Yu, F Wang, Y Li, G Zhang, S Tao, H Li, R Sang, X Zhao, C Li, Wang Wang, M, J Yang, C Xin, G Yin, J Li, Z Xie, B Wang, C Zheng, Y Qu, J Xu, B Wang, Yanjun Hu, Xiping Zhang, Shuai Zhao","doi":"10.22514/ejgo.2024.007","DOIUrl":"https://doi.org/10.22514/ejgo.2024.007","url":null,"abstract":"Breast cancer (BCa) is a prevalent form of tumor, necessitating the development of more effective therapeutic drugs to improve patient prognosis. Taraxasterol (TAX), derived from the dandelion plant, has demonstrated significant physiological and pharmacological activity, but its role in BCa and underlying mechanism remains unexplored. In this study, we investigate the effects of TAX on the growth, motility and apoptosis of BCa cells in vitro to determine its mechanistic actions. Our results demonstrate that TAX significantly reduces both the proliferation and motility of BCa cells and induces apoptosis in BCa cells, as confirmed through flow cytometry (FCM). This apoptotic effect was further supported by JC-1 staining, which showed alterations in mitochondrial membrane potential in BCa cells after TAX treatment. Mechanistically, TAX suppresses the phosphatidylinositide 3-kinases/protein kinase B (PI3K/AKT) and EGFR pathways and impedes BCa progression. Collectively, TAX stimulates BCa cell apoptosis by inhibiting the PI3K/AKT and EGFR pathways.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 1","pages":"42-42"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://oss.ejgo.net/files/article/20240206-269/pdf/EJGO2023083101.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147885310","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":"ZNF671 restrains endometrial cancer cell growth and stemness through the Wnt/β-catenin pathway","authors":"","doi":"10.22514/ejgo.2024.077","DOIUrl":"https://doi.org/10.22514/ejgo.2024.077","url":null,"abstract":"Endometrial cancer is a common malignant cancer in women, which poses serious health risks. Multifarious cancers have been shown to be suppressed by Zinc finger protein 671 (ZNF671). However, the precise regulatory impact of ZNF671 on endometrial cancer progression remains unclear. This study investigated ZNF671’s role in endometrial cancer. The Ualcan online database revealed that ZNF671 exhibited low expression in uterine corpus endometrial carcinoma (UCEC) tissues. Endometrial cancer patients who exhibited low ZNF671 expression suffered poor prognosis. ZNF671 also retarded tumor growth in endometrial cancer. Cell invasion and migration were restrained by ZNF671. In addition, ZNF671 inhibited endometrial cancer stemness. Eventually, ZNF671 suppressed the Wnt/β-catenin pathway. In conclusion, ZNF671 restrained both cell growth and stemness in endometrial cancer through the Wnt/β-catenin pathway. ZNF671 may serve as a bio-target for endometrial cancer treatment.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 4","pages":"125-125"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147922573","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":"FOXK2 affects the motility of endometrial cancer cells by mediating ZEB1","authors":"","doi":"10.22514/ejgo.2024.130","DOIUrl":"https://doi.org/10.22514/ejgo.2024.130","url":null,"abstract":"Endometrial cancer (EC) is a prevalent type of malignancy, highlighting the need for the development of effective therapies and the identification of novel therapeutic targets. FOXK2, a member of the Foxhead box (FOX) family, has been implicated in cancer progression. However, the role of FOXK2 in EC and its underlying mechanisms remain poorly understood. This study investigates the function of FOXK2 in EC. FOXK2 is significantly overexpressed in EC tissues. Knockdown of FOXK2 impedes the proliferation of EC cells and inhibits their motility and epithelial-mesenchymal transition (EMT). Mechanistically, FOXK2 depletion disrupts EC progression by targeting Zinc Finger E-Box Binding Homeobox 1 (ZEB1). In conclusion, FOXK2 regulates EC cell progression through modulation of ZEB1.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 6","pages":"164-164"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147898466","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":"Magnoflorine inhibits cisplatin-induced protective autophagy by down-regulating HMGB1 and increases drug sensitivity in drug-resistant ovarian cancer cells","authors":"Shujun Zhang, Xin He, Lei Fan, Qianru Zhang, B Gloss, K Moran-Jones, V Lin, M Gonzalez, J Scurry, N Hacker, B Pickwell-Smith, S Greenley, M Lind, U Macleod, Y Ma, Z Wei, R Bast, Z Wang, Y Li, M Gao, H He, Y Feng, L Zang, W Liu, L Ding, L Chen, J He, G Zhang, Q Pang, C Yu, J Xiong, J Zhu, J Tan, X Jiang, G Yin, L He, J Liu, Z Long, T Ghezelayagh, E Wu, E Barber, M Dao, E Zsiros, R Urban, C Chen, L Dai, M Wang, X Lai, J Wang, J Zhu, S Lin, X Zou, X Chen, Y Liu, X Yang, E Okon, W Kukula-Koch, M Halasa, A Jarzab, M Baran, M Dmoszynska-Graniczka, A Yadav, A Singh, J Phogat, A Dahuja, R Dabur, X Sun, X Zhang, H Zhai, D Zhang, S Ma, T Wei, X Xiaojun, C Peilong, T Xu, L Jiang, Z Wang, A Burges, B Schmalfeldt, L Zhong, Y Qin, M Liu, J Sun, H Tang, Y Zeng, L Wang, P Li, Y Zhou, R Gu, G Lu, C Zhang, L Zhang, Y Liu, X Lei, X Liu, H Sun, S Liu, Y Zhou, T Liu, Q Wu, H Wang, Y Sun, M Baran, P Miziak, K Bonio","doi":"10.22514/ejgo.2024.018","DOIUrl":"https://doi.org/10.22514/ejgo.2024.018","url":null,"abstract":"Ovarian cancer (OC) is a prevalent type of gynecologic malignancy, and to improve its treatment effectiveness, it is essential to identify new and more potent therapeutic drugs. Magnoflorine is a fundamental chlorine alkaloid with various pharmacological properties, including anti-diabetic and anti-inflammatory effects. However, whether Magnoflorine can inhibit the protective autophagy induced by cisplatin by modulating (high-mobility group B1) HMGB1 requires further investigation. This study aims to assess the impact of Magnoflorine on cisplatin resistance in OC. Our findings demonstrate that Magnoflorine enhances the sensitivity of OC cells to cisplatin. Additionally, it promotes apoptosis in cisplatin-resistant OC cells and simultaneously inhibits cisplatin-induced protective autophagy. Mechanistically, Magnoflorine reduces HMGB1 expression in cisplatin-resistant OC cells. Collectively, these results suggest that Magnoflorine has potential as a therapeutic agent for cisplatin-resistant OC in future clinical applications.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 1","pages":"132-132"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://oss.ejgo.net/files/article/20240206-285/pdf/EJGO2023100701.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147885679","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":"Meis1 restrains the growth and epithelial-mesenchymal transition of breast cancer cells through the HOXB13/PI3K/AKT signaling pathway","authors":"","doi":"10.22514/ejgo.2024.124","DOIUrl":"https://doi.org/10.22514/ejgo.2024.124","url":null,"abstract":"Breast cancer (BC) is one hackneyed malignant tumor occurred on breast in female and possesses a higher mortality. Meis1 serves as a homeobox (HOX)-family transcription factor, and has been disclosed to take part into the modulation of diseases’ progression. However, the detailed impacts and associated regulatory pathway of Meis1 in BC progression keep dimness. The protein expressions were inspected through western blot. The cell viability and proliferation were determined through cell counting kit-8 (CCK-8) and colony formation assays. The cell apoptosis was determined through flow cytometry. The cellular morphological changes were verified through Phalloidin staining. The interaction between Meis1 and HOXB13 was confirmed through co-immunoprecipitation (Co-IP) assay. In this study, Meis1 expression was down-regulated in BRCA (breast invasive carcinoma) tissues from gene expression profiling interactive analysis (GEPIA) online database. And, it was uncovered that Meis1 existed the lower expression in BC cell lines. Besides, amplification of Meis1 restrained cell growth and aggrandized cell apoptosis in BC. Additionally, augmentation of Meis1 weakened epithelial-mesenchymal transition (EMT) process in BC through augmenting E-cadherin as well as declining neural cadherin (N-cadherin) and α-smooth muscle actin (α-SMA) expressions. Lastly, it was uncovered that overexpression of Meis1 retarded the HOXB13/phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway. To sum up, this study revealed that Meis1 restrained cell proliferation and epithelial-mesenchymal transition (EMT) process in BC through the HOXB13/PI3K/AKT signaling pathway. This work suggested that Meis1 may be one available molecular target for the amelioration of BC.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 6","pages":"117-117"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147886079","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":"Beta-Caryophyllene can inhibit the proliferation and autophagy of HPV16-infected immortalized cervical epithelial cells","authors":"","doi":"10.22514/ejgo.2024.073","DOIUrl":"https://doi.org/10.22514/ejgo.2024.073","url":null,"abstract":"Cervical cancer arises due to the progressive dysplasia of cervical epithelial cells, characterized pathologically as cervical intraepithelial neoplasia (CIN). Given the urgency for effective treatments against CIN, exploring novel pharmaceutical candidates is of paramount importance. Beta-Caryophyllene (BCP), derived from various plants, has shown promise in impeding the progression of various malignancies. However, its potential efficacy in CIN treatment remains unexplored. In this study, we investigate the impact of BCP on CIN progression and elucidate its mechanism of action. An immortalized cervical epithelial cell line (H8) infected with HPV16 was used as a model for CIN. The results revealed that BCP significantly inhibited the proliferation of H8 cells and induced apoptosis. Moreover, BCP demonstrated the ability to suppress autophagy in H8 cells. Mechanistically, our findings indicate that BCP exerts its effects by modulating the Wnt/β-catenin signaling pathway. Specifically, BCP was found to block this pathway, thereby impeding cell growth and autophagy in H8 cells. These results suggest that BCP holds promise as a therapeutic agent for CIN, potentially through its regulatory effects on the Wnt/β-catenin pathway.","PeriodicalId":11903,"journal":{"name":"European journal of gynaecological oncology","volume":"45 4","pages":"93-93"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147892653","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}