NCAPH promotes glucose metabolism reprogramming and cell stemness in ovarian cancer cells through the MEK/ERK/PD-L1 pathway.

IF 3.8 3区医学 Q1 REPRODUCTIVE BIOLOGY

Journal of Ovarian Research Pub Date : 2025-04-21 DOI:10.1186/s13048-025-01659-6

Yingying Qi, Aiping Wang, Silin Chen, Wei Chen

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引用次数: 0

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.

查看原文本刊更多论文

NCAPH通过MEK/ERK/PD-L1通路促进卵巢癌细胞的糖代谢重编程和细胞干细胞。

背景：卵巢癌是一种影响女性生殖系统的常见恶性肿瘤，具有高度异质性。染色体凝聚素I复合体亚基H （NCAPH）的非结构维持与多种癌症有关。方法：采用RT-qPCR和western blot分析转染前后NCAPH的表达情况。通过球体形成试验评价细胞的干细胞性。采用海马糖酵解应激试验测定卵巢癌细胞胞外酸化率（ECAR），采用海马水户应激试验测定耗氧量（OCR）。采用相应的检测试剂盒定量测定乳酸生成和葡萄糖消耗。Western blot分析干细胞标志物、糖酵解和MEK/ERK/PD-L1信号通路相关蛋白的表达。在体内记录肿瘤大小和重量，免疫组化染色检测裸鼠肿瘤组织中MEK/ERK/PD-L1和KI67的表达。结果：NCAPH在卵巢癌细胞中表达上调。沉默NCAPH导致茎秆特性和糖代谢重编程的抑制。此外，在体外和体内实验中，敲低NCAPH可抑制MEK/ERK/PD-L1信号通路，从而抑制小鼠模型中的肿瘤生长。结论：总的来说，沉默NCAPH通过调节MEK/ERK/PD-L1通路阻碍卵巢癌的恶性进展。临床试验号：不适用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Ovarian Research REPRODUCTIVE BIOLOGY-

CiteScore

6.20

自引率

2.50%

发文量

125

审稿时长

>12 weeks

期刊介绍： Journal of Ovarian Research is an open access, peer reviewed, online journal that aims to provide a forum for high-quality basic and clinical research on ovarian function, abnormalities, and cancer. The journal focuses on research that provides new insights into ovarian functions as well as prevention and treatment of diseases afflicting the organ. Topical areas include, but are not restricted to: Ovary development, hormone secretion and regulation Follicle growth and ovulation Infertility and Polycystic ovarian syndrome Regulation of pituitary and other biological functions by ovarian hormones Ovarian cancer, its prevention, diagnosis and treatment Drug development and screening Role of stem cells in ovary development and function.