研究动态
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Caveolin-1 依赖性生腱蛋白 C 包含在细胞外囊泡中是促进乳腺癌细胞恶性的必要条件。

Caveolin-1-dependent tenascin C inclusion in extracellular vesicles is required to promote breast cancer cell malignancy.

发表日期:2023 Nov 06
作者: America Campos, Renato Burgos-Ravanal, Lorena Lobos-González, Ricardo Huilcamán, María Fernanda González, Jorge Díaz, Albano Cáceres Verschae, Juan Pablo Acevedo, Macarena Carrasco, Francisca Sepúlveda, Emanuel Jeldes, Manuel Varas-Godoy, Lisette Leyton, Andrew Fg Quest
来源: Cellular & Molecular Immunology

摘要:

背景:乳腺癌中 CAV1 表达升高会加速肿瘤进展。来自表达 CAV1 的 MDA-MB-231 乳腺癌细胞的细胞外囊泡 (EV) 含有腱蛋白 C (TNC),但 TNC 的相关性仍有待确定。方法:通过纳米追踪分析、显微镜和蛋白质印迹对 EV 进行表征。使用流式细胞术研究细胞对 EV 的摄取。通过迁移、侵袭、集落形成和体内试验测试了 EV 对乳腺癌细胞的影响。结果:EV被细胞吸收;然而,只有含有 TNC 的物质才会促进侵袭性。在体内,缺乏 TNC 的 EV 不再促进肿瘤生长。结论:乳腺癌细胞来源的 EV 中含有的 CAV1 和 TNC 被确定为有利于乳腺癌进展的蛋白质。
Background: Elevated expression of CAV1 in breast cancer increases tumor progression. Extracellular vesicles (EVs) from CAV1-expressing MDA-MB-231 breast cancer cells contain Tenascin C (TNC), but the relevance of TNC remained to be defined. Methods: EVs were characterized by nanotracking analysis, microscopy and western blotting. The uptake of EVs by cells was studied using flow cytometry. The effects of EVs on breast cancer cells were tested in migration, invasion, colony formation and in vivo assays. Results: EVs were taken up by cells; however, only those containing TNC promoted invasiveness. In vivo, EVs lacking TNC ceased to promote tumor growth. Conclusion: CAV1 and TNC contained in breast cancer cell-derived EVs were identified as proteins that favor progression of breast cancer.