NCAPH promotes glucose metabolism reprogramming and cell stemness in ovarian cancer cells through the MEK/ERK/PD-L1 pathway
Abstract Backgrounds Ovarian cancer is a prevalent malignant tumor that affects the female reproductive system with the characteristic of high heterogeneity. Non-structural maintenance of chromosomes condensin I complex subunit H (NCAPH) has been implicated in a variety of cancers. Methods The expre...
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| Language: | English |
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BMC
2025-04-01
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| Series: | Journal of Ovarian Research |
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| Online Access: | https://doi.org/10.1186/s13048-025-01659-6 |
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| author | Yingying Qi Aiping Wang Silin Chen Wei Chen |
| author_facet | Yingying Qi Aiping Wang Silin Chen Wei Chen |
| author_sort | Yingying Qi |
| collection | DOAJ |
| description | Abstract Backgrounds Ovarian cancer is a prevalent malignant tumor that affects the female reproductive system with the characteristic of high heterogeneity. Non-structural maintenance of chromosomes condensin I complex subunit H (NCAPH) has been implicated in a variety of cancers. Methods The expression of NCAPH before and after transfection were assessed using RT-qPCR and western blot analysis. Cell stemness was evaluated through spheroid formation assay. The extracellular acidification rate (ECAR) of ovarian cancer cells was measured utilizing Seahorse Glycolysis Stress Test Assay while oxygen consumption rate (OCR) was estimated with Seahorse Mito Stress Test Assay. Lactate production and glucose consumption were quantified using corresponding assay kits. Western blot was employed to analyze the expression of stem cell markers, glycolysis- and MEK/ERK/PD-L1 signaling pathway-related proteins. In vivo, tumor size and weight were recorded, and immunohistochemical staining was used to assess MEK/ERK/PD-L1 and KI67 expression in tumor tissues from nude mice. Results It was observed that NCAPH expression is upregulated in ovarian cancer cells. Silencing NCAPH led to repression of both stemness characteristics and glucose metabolism reprogramming. Furthermore, knockdown of NCAPH inhibited the MEK/ERK/PD-L1 signaling pathway both in vitro and in vivo, resulting in suppressed tumor growth in mouse models. Conclusion Collectively, silencing NCAPH impedes malignant progression of ovarian cancer through modulation of the MEK/ERK/PD-L1 pathway. Clinical trial number Not applicable. |
| format | Article |
| id | doaj-art-81bac3afb1504478b527aeea67cf80b4 |
| institution | DOAJ |
| issn | 1757-2215 |
| language | English |
| publishDate | 2025-04-01 |
| publisher | BMC |
| record_format | Article |
| series | Journal of Ovarian Research |
| spelling | doaj-art-81bac3afb1504478b527aeea67cf80b42025-08-20T03:15:14ZengBMCJournal of Ovarian Research1757-22152025-04-0118111110.1186/s13048-025-01659-6NCAPH promotes glucose metabolism reprogramming and cell stemness in ovarian cancer cells through the MEK/ERK/PD-L1 pathwayYingying Qi0Aiping Wang1Silin Chen2Wei Chen3Department of Gynecology, The Fifth Affiliated Hospital of Guangzhou Medical UniversityDepartment of Gynecology, The Fifth Affiliated Hospital of Guangzhou Medical UniversityDepartment of Gynecology, The Fifth Affiliated Hospital of Guangzhou Medical UniversityDepartment of Gynecology, The Fifth Affiliated Hospital of Guangzhou Medical UniversityAbstract Backgrounds Ovarian cancer is a prevalent malignant tumor that affects the female reproductive system with the characteristic of high heterogeneity. Non-structural maintenance of chromosomes condensin I complex subunit H (NCAPH) has been implicated in a variety of cancers. Methods The expression of NCAPH before and after transfection were assessed using RT-qPCR and western blot analysis. Cell stemness was evaluated through spheroid formation assay. The extracellular acidification rate (ECAR) of ovarian cancer cells was measured utilizing Seahorse Glycolysis Stress Test Assay while oxygen consumption rate (OCR) was estimated with Seahorse Mito Stress Test Assay. Lactate production and glucose consumption were quantified using corresponding assay kits. Western blot was employed to analyze the expression of stem cell markers, glycolysis- and MEK/ERK/PD-L1 signaling pathway-related proteins. In vivo, tumor size and weight were recorded, and immunohistochemical staining was used to assess MEK/ERK/PD-L1 and KI67 expression in tumor tissues from nude mice. Results It was observed that NCAPH expression is upregulated in ovarian cancer cells. Silencing NCAPH led to repression of both stemness characteristics and glucose metabolism reprogramming. Furthermore, knockdown of NCAPH inhibited the MEK/ERK/PD-L1 signaling pathway both in vitro and in vivo, resulting in suppressed tumor growth in mouse models. Conclusion Collectively, silencing NCAPH impedes malignant progression of ovarian cancer through modulation of the MEK/ERK/PD-L1 pathway. Clinical trial number Not applicable.https://doi.org/10.1186/s13048-025-01659-6Ovarian cancerNCAPHMEK/ERK/PD-L1 pathwayGlucose metabolism reprogrammingStemness |
| spellingShingle | Yingying Qi Aiping Wang Silin Chen Wei Chen NCAPH promotes glucose metabolism reprogramming and cell stemness in ovarian cancer cells through the MEK/ERK/PD-L1 pathway Journal of Ovarian Research Ovarian cancer NCAPH MEK/ERK/PD-L1 pathway Glucose metabolism reprogramming Stemness |
| title | NCAPH promotes glucose metabolism reprogramming and cell stemness in ovarian cancer cells through the MEK/ERK/PD-L1 pathway |
| title_full | NCAPH promotes glucose metabolism reprogramming and cell stemness in ovarian cancer cells through the MEK/ERK/PD-L1 pathway |
| title_fullStr | NCAPH promotes glucose metabolism reprogramming and cell stemness in ovarian cancer cells through the MEK/ERK/PD-L1 pathway |
| title_full_unstemmed | NCAPH promotes glucose metabolism reprogramming and cell stemness in ovarian cancer cells through the MEK/ERK/PD-L1 pathway |
| title_short | NCAPH promotes glucose metabolism reprogramming and cell stemness in ovarian cancer cells through the MEK/ERK/PD-L1 pathway |
| title_sort | ncaph promotes glucose metabolism reprogramming and cell stemness in ovarian cancer cells through the mek erk pd l1 pathway |
| topic | Ovarian cancer NCAPH MEK/ERK/PD-L1 pathway Glucose metabolism reprogramming Stemness |
| url | https://doi.org/10.1186/s13048-025-01659-6 |
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