长链非编码RNA（lncRNA）的出现被证明对于致命的女性恶性肿瘤三阴性乳腺癌（TNBC）的恶化至关重要。 LINC00668 此前曾作为 TNBC 中过表达的 lncRNA 被发现。然而，其确切功能以及是否在 TNBC 开发中发挥作用还需要确定。为了探索这一点，使用 qRT-PCR 来检测 TNBC 细胞中的失调。 LINC00668的生物学功能是通过功能丧失实验确定的。利用生物信息学分析来预测LINC00668的下游调节基因。采用双荧光素酶报告基因测定加上 RNA 免疫沉淀分析、定量 PCR 分析和救援测定来探索模式在竞争性内源 RNA (ceRNA) 网络中的潜在作用。研究表明，LINC00668 表达上调，其缺失导致 TNBC 细胞增殖和迁移受阻。生物信息学分析和机械测定发现，LINC00668 海绵 miR-518c-3p 促进 TNBC 中 WDR1 水平。此外，救援实验表明，LINC00668/miR-518c-3p 通路以 WDR1 依赖性的形式促进 TNBC 细胞增殖和迁移。总的来说，我们的研究可能会发现 TNBC 患者 lncRNA 定向治疗治愈的重要线索。版权所有 © 2024。由 Elsevier B.V. 出版。

The emergence of long noncoding RNAs (lncRNAs) was proved to be crucial to the aggravation of triple negative breast cancer (TNBC), a fatal female malignancy. LINC00668 was unveiled as an overexpressed lncRNA in TNBC previously. However, its exact function and whether it functioned in TNBC development needs to be ascertained. To explore this, qRT-PCR was used to detect its dysregulation in TNBC cells. Biological functions of LINC00668 were determined through loss-of-function experiments. Bioinformatics analysis was utilized to predict the downstream modulatory genes of LINC00668. Dual-luciferase reporter assay plus RNA immunoprecipitation analysis, quantitative PCR analysis, and rescue assays were employed for the exploration of potential action of mode in competitive endogenous RNA (ceRNA) network. It was revealed that LINC00668 was upregulated and its depletion resulted in impeded proliferation and migration of TNBC cells. Bioinformatics analysis and mechanical assays uncovered that LINC00668 sponged miR-518c-3p to facilitate WDR1 level in TNBC. Furthermore, rescue experiments demonstrated that LINC00668/miR-518c-3p pathway contributed to TNBC cell proliferation and migration in the form of WDR1 dependency. Overall our study might discover a vital clue for the cure of lncRNA-directed treatment for TNBC patients.Copyright © 2024. Published by Elsevier B.V.