IF 3.5 2区 生物学 Q3 CELL BIOLOGY Molecular and Cellular Biochemistry Pub Date : 2025-02-01 DOI:10.1007/s11010-025-05216-z
Fu Hua, YunLang Cai
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引用次数: 0

摘要

子宫内膜癌(EC)是子宫内膜上皮的恶性肿瘤。该病的发病率和死亡率在全球呈上升趋势。我们采集了20例I型子宫内膜癌组织进行转录组测序,结果表明PAX2在子宫内膜癌组织中高表达,并与子宫内膜癌的发病机制密切相关。PAX2 是成对同源染色体结构域家族的成员,与多种不同肿瘤的发病有关。在正常的子宫内膜组织中,PAX2 是甲基化的;但在子宫内膜癌中,它是去甲基化的。然而,很少有研究关注它在子宫内膜癌中的作用。蛋白-蛋白相互作用(PPI)分析表明,PAX2 与 CD133 之间存在调控关系,而 CD133 又会影响 AKT1 的活性。CD133 是众所周知的肿瘤干细胞标记物,参与肿瘤的发生、转移、复发和耐药性;AKT1 通过抑制细胞凋亡促进细胞存活,被认为是多种癌症的主要促进因子。然而,PAX2 是否会通过调控 CD133-AKT1 通路影响癌细胞的进展还需要进一步研究。本研究表明,PAX2 能促进细胞增殖、迁移、侵袭和粘附,并抑制细胞凋亡。其作用机制是抑制线粒体氧化磷酸化、促进糖酵解、增加线粒体拷贝数、增加活性氧(ROS)和己糖激酶水平以及线粒体钙离子浓度。这是通过促进 CD133 的表达和 AKT1 的磷酸化实现的。结合上述调控途径,促进了心肌梗死的进展。
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PAX2 induces endometrial cancer by inhibiting mitochondrial function via the CD133-AKT1 pathway.

Endometrial cancer (EC) is a malignancy of the endometrial epithelium. The prevalence and mortality rates associated with the disease are on the rise globally. A total of 20 cases of type I EC tissues were collected for transcriptomic sequencing, our findings indicate that PAX2 is highly expressed in EC tissues and is closely related to the pathogenesis of EC. PAX2 is a member of the paired homeobox domain family and has been linked to the development of a number of different tumours. In normal endometrial tissue, PAX2 is methylated; however, in EC, it is demethylated. Nevertheless, few studies have focused on its role in EC. A protein-protein interaction (PPI) analysis revealed a regulatory relationship between PAX2 and CD133, which in turn affects the activity of AKT1. CD133 is a well-known marker of tumor stem cells and is involved in tumor initiation, metastasis, recurrence, and drug resistance; AKT1 promotes cell survival by inhibiting apoptosis and is considered a major promoter of many types of cancer. Nevertheless, further investigation is required to ascertain whether PAX2 affects the progression of EC by regulating the CD133-AKT1 pathway. The present study demonstrated that PAX2 promoted cell proliferation, migration, invasion and adhesion, and inhibited apoptosis. Its mechanism of action was found to be the inhibition of mitochondrial oxidative phosphorylation, promotion of glycolysis, increase in mitochondrial copy number, and increase in the levels of reactive oxygen species (ROS) and hexokinase, as well as the concentration of mitochondrial calcium ions. This was achieved through the promotion of CD133 expression and the phosphorylation of AKT1. In conjunction with the aforementioned regulatory pathways, the progression of EC is facilitated.

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来源期刊
Molecular and Cellular Biochemistry
Molecular and Cellular Biochemistry 生物-细胞生物学
CiteScore
8.30
自引率
2.30%
发文量
293
审稿时长
1.7 months
期刊介绍: Molecular and Cellular Biochemistry: An International Journal for Chemical Biology in Health and Disease publishes original research papers and short communications in all areas of the biochemical sciences, emphasizing novel findings relevant to the biochemical basis of cellular function and disease processes, as well as the mechanics of action of hormones and chemical agents. Coverage includes membrane transport, receptor mechanism, immune response, secretory processes, and cytoskeletal function, as well as biochemical structure-function relationships in the cell. In addition to the reports of original research, the journal publishes state of the art reviews. Specific subjects covered by Molecular and Cellular Biochemistry include cellular metabolism, cellular pathophysiology, enzymology, ion transport, lipid biochemistry, membrane biochemistry, molecular biology, nuclear structure and function, and protein chemistry.
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