越来越多的证据表明，细粒棘球绦虫幼虫阶段的分泌/排泄抗原可以诱导寄生虫衍生代谢物与各种癌细胞之间的抗癌和致癌作用。 miR-145 作为肿瘤抑制基因或癌基因的双重作用已在癌症中得到报道。然而，miR-145 诱导包虫囊液 (HCF) 处理的肺癌细胞凋亡的机制仍不清楚。可育的 HCF 是从绵羊身上获得的，经过纯化和冻干。然后将H1299人肺癌细胞培养成两组：HCF处理的H1299肺癌细胞和作为对照细胞的未处理的H1299癌细胞。使用MTT测定评估细胞活力以评估HCF对H1299细胞的影响。 Caspase-3 活性通过荧光测定进行评估。此外，通过实时 PCR 定量 VGEF、vimentin、caspase-3、miRNA-145、Bax 和 Bcl-2 基因的 mRNA 表达水平。还进行了划痕测试以评估 HCF 对细胞迁移的影响。 MTT分析显示，当用60μg/mL的可育HCF处理24小时时，H1299细胞的生长增加。与对照细胞相比，HCF 处理的 H1299 细胞中 caspase-3、miRNA-145、Bax/Bcl-2 比率和 caspase-3 活性的倍数变化较低。 HCF 处理的 H1299 细胞中 VGEF 和波形蛋白基因表达的倍数变化高于对照细胞。划痕测试结果显示，暴露于HCF 24和48小时后，H1299细胞迁移率增加。我们的结果表明，HCF 处理的 H1299 细胞中 miR-145 的下调可能作为肺癌生长的致癌调节因子发挥作用。为了证实这一假设，需要进一步研究来评估 microRNA 谱和体内有效致癌基因。版权所有 © 2024。由 Elsevier Inc. 出版。

There is increasing evidence that the secretory/excretory antigens of the larval stage of Echinococcus granulosus can induce both anticancer and oncogenic effects between parasite-derived metabolites and various cancer cells. The dual role of miR-145 as either a tumor suppressor or oncogene has already been reported in cancer. However, the mechanism by which miR-145 induces apoptosis in lung cancer cells treated with hydatid cyst fluid (HCF) remains unclear. The fertile HCF was obtained from sheep, purified and lyophilized. H1299 human lung cancer cells were then cultured into two groups: HCF-treated H1299 lung cancer cells and untreated H1299 cancer cells as control cells. Cell viability was assessed using MTT assay to evaluate the effects of HCF on the H1299 cells. Caspase-3 activity was assessed by fluorometric assay. In addition, mRNA expression levels of VGEF, vimentin, caspase-3, miRNA-145, Bax and Bcl-2 genes were quantified by real-time PCR. A scratch test was also performed to assess the effects of HCF on cell migration. The MTT assay revealed that the growth of H1299 cells increased when treated with 60 μg/mL of fertile HCF for 24 hours. The fold change of caspase-3, miRNA-145, Bax/Bcl-2 ratio and caspase-3 activity was lower in HCF-treated H1299 cells compared to the control cell. The fold change in VGEF and vimentin gene expression was higher in the HCF-treated H1299 cells than in the control cell. The scratch test results showed that H1299 cell mobility increased 24 and 48 hours after exposure to HCF. Our results suggest that the downregulation of miR-145 in HCF-treated H1299 cells may play a role as a possible oncogenic regulator of lung cancer growth. To confirm this assumption, further studies are required to evaluate the microRNA profile and effective oncogenes in vivo.Copyright © 2024. Published by Elsevier Inc.