Kulinska Karolina Iwona, Wierzbicka Magdalena, Dera-Szymanowska Anna, Szymanowski Krzysztof, Andrusiewicz Mirosław, Wołuń-Cholewa Maria
Department of Cell Biology, Poznan University of Medical Sciences, 60-806 Poznań, Poland.
Clinic of Perinatology and Gynaecology, Poznan University of Medical Sciences, 60-535 Poznań, Poland.
Biomedicines. 2025 Jan 10;13(1):158. doi: 10.3390/biomedicines13010158.
: Endometriosis is a painful chronic condition in which the endometrium grows outside the uterus. The epithelial-mesenchymal transition (EMT) is critical to endometriosis progression, where cells lose epithelial traits and gain invasiveness. : This study investigates the effects of phoenixin-14 (PNX-14), a neuropeptide found at reduced levels in endometriosis patients, on the expression of two molecular EMT markers, CDH1 (E-cadherin) and THBS2 (thrombospondin 2), as well as cell viability in the endometriosis-derived 12Z cell line. Cells were treated with physiological (0.2 nM) and endometriosis-relevant (0.05 nM) concentrations of PNX-14. Gene expression was analyzed using RT-qPCR, while protein localization was assessed by immunocytochemistry. Cell viability was measured using an XTT assay. : gene expression was significantly decreased, and remained unchanged in cells stimulated by 0.05 nM PNX-14. Immunolocalization indicates a weaker THBS2 and CDH1 protein immunosignal reaction for 0.05 nM PNX-14. PNX-14 treatment also exhibited a biphasic effect on cell viability. Lower concentration initially decreased viability at 48 h but then significantly increased it at 72 h. This increase coincided with the decrease in expression, suggesting a potential link between PNX-14, , and cell viability. : A negative correlation between cell viability and the expression of both EMT markers further highlights their possible involvement in the survival and adaptability of ectopic epithelial cells. Our findings suggest a complex interplay between PNX-14, EMT markers, and cell viability in ectopic epithelial cells. PNX-14's ability to modulate these factors warrants further investigation to elucidate its role in endometriosis.
子宫内膜异位症是一种痛苦的慢性疾病，其中子宫内膜在子宫外生长。上皮-间质转化（EMT）对于子宫内膜异位症的进展至关重要，在此过程中细胞失去上皮特征并获得侵袭性。本研究调查了在子宫内膜异位症患者中水平降低的神经肽凤肽-14（PNX-14）对子宫内膜异位症来源的12Z细胞系中两种分子EMT标志物CDH1（E-钙黏蛋白）和THBS2（血小板反应蛋白2）的表达以及细胞活力的影响。细胞用生理浓度（0.2 nM）和与子宫内膜异位症相关的浓度（0.05 nM）的PNX-14处理。使用RT-qPCR分析基因表达，同时通过免疫细胞化学评估蛋白质定位。使用XTT测定法测量细胞活力。在0.05 nM PNX-14刺激的细胞中，基因表达显著降低，而 保持不变。免疫定位表明0.05 nM PNX-14的THBS2和CDH1蛋白免疫信号反应较弱。PNX-14处理对细胞活力也表现出双相作用。较低浓度最初在48小时时降低活力，但随后在72小时时显著增加。这种增加与 表达的降低同时发生，表明PNX-14、 和细胞活力之间可能存在联系。细胞活力与两种EMT标志物的表达之间的负相关进一步突出了它们可能参与异位上皮细胞的存活和适应性。我们的研究结果表明在异位上皮细胞中PNX-14、EMT标志物和细胞活力之间存在复杂的相互作用。PNX-14调节这些因素的能力值得进一步研究以阐明其在子宫内膜异位症中的作用。
