越来越多的证据表明血小板在卵巢癌的发生和进展中发挥作用，卵巢癌是一种由输卵管引起的高度致命的疾病，目前尚无早期检测或预防的方法。血栓形成是卵巢癌患者死亡的主要原因，表明癌症改变了血小板行为。本研究的目的是开发人血小板和卵巢癌细胞病理相互作用的细胞培养模型，使用正常 FT 上皮细胞作为健康对照，并测试抗血小板二高-γ-亚麻酸的效果。 DGLA）在模型中。健康细胞和癌细胞都会引起血小板聚集，但血小板只影响癌细胞球体的形成，对健康细胞球体的形成没有影响。当自然形成的上皮细胞球体暴露于不允许两种细胞类型直接相互作用的transwell插入物中的血小板时，血小板导致癌细胞形成的球体尺寸增加，但不增加健康细胞形成的球体尺寸。当使用磁性纳米梭技术形成的癌细胞球体与血小板直接物理接触时，血小板引起球体凝结。在卵巢癌细胞中，DGLA 在低至 100 μM 的剂量下可促进上皮间质 (EMT) 转变，在 ≥150 μM 的剂量下可抑制代谢活力并诱导细胞凋亡。 DGLA剂量≤150μM用于避免DGLA对癌细胞的直接影响，对我们模型中血小板和卵巢癌细胞的病理相互作用没有影响。这些结果表明，血小板与卵巢癌细胞的病理相互作用可以在细胞培养中建模，并且 DGLA 对这些相互作用没有影响，这表明靶向血小板是降低卵巢癌患者癌症侵袭性和血栓形成风险的合理方法。然而，DGLA 并不是该策略的合适候选者。版权所有：© 2024 Isingizwe 等人。这是一篇根据知识共享署名许可条款分发的开放获取文章，允许在任何媒体上不受限制地使用、分发和复制，前提是注明原始作者和来源。

Increasing evidence is implicating roles for platelets in the development and progression of ovarian cancer, a highly lethal disease that can arise from the fallopian tubes, and has no current method of early detection or prevention. Thrombosis is a major cause of mortality of ovarian cancer patients suggesting that the cancer alters platelet behavior. The objective of this study was to develop a cell culture model of the pathological interactions of human platelets and ovarian cancer cells, using normal FT epithelial cells as a healthy control, and to test effects of the anti-platelet dihomo-gamma-linolenic acid (DGLA) in the model. Both healthy and cancer cells caused platelet aggregation, however platelets only affected spheroid formation by cancer cells and had no effect on healthy cell spheroid formation. When naturally-formed spheroids of epithelial cells were exposed to platelets in transwell inserts that did not allow direct interactions of the two cell types, platelets caused increased size of the spheroids formed by cancer cells, but not healthy cells. When cancer cell spheroids formed using magnetic nanoshuttle technology were put in direct physical contact with platelets, the platelets caused spheroid condensation. In ovarian cancer cells, DGLA promoted epithelial-to-mesenchymal (EMT) transition at doses as low as 100 μM, and inhibited metabolic viability and induced apoptosis at doses ≥150 μM. DGLA doses ≤150 μM used to avoid direct DGLA effects on cancer cells, had no effect on the pathological interactions of platelets and ovarian cancer cells in our models. These results demonstrate that the pathological interactions of platelets with ovarian cancer cells can be modeled in cell culture, and that DGLA has no effect on these interactions, suggesting that targeting platelets is a rational approach for reducing cancer aggressiveness and thrombosis risk in ovarian cancer patients, however DGLA is not an appropriate candidate for this strategy.Copyright: © 2024 Isingizwe et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.