一种新鉴定的长链非编码 RNA，LINC01574，通过调节 miR-6745/TTYH3 轴促进乳腺癌恶化。
A Novel Identified Long Intergenic Noncoding RNA, LINC01574, Contributes to Breast Cancer Deterioration via the Regulation of miR-6745/TTYH3 Axis.
机构信息
School of Medicine, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China.
Department of Breast and Thyroid Surgery, Shandong Provincial Maternal and Child Health Care Hospital, Jinan, Shandong 250014, China.
出版信息
J Immunol Res. 2022 Jul 27;2022:4201283. doi: 10.1155/2022/4201283. eCollection 2022.
OBJECTIVE
Compelling evidence suggested that lncRNAs performed vital functions in the development of breast cancer (BC). The study intended to mine the functional roles of LINC01574 in BC and further excavated its underlying regulatory mechanism.
METHODS
The expression and prognosis of LINC01574 in BC were detected by integrating analysis of data mining, bioinformatics, and RT-qPCR. Then, the effect of LINC01574 knockdown on BC cell growth and metastasis was evaluated in vitro and in vivo. Interactions between miR-6745 and LINC01574 or TTYH3 were revealed by both target prediction and dual luciferase reporter assay.
RESULTS
Our data found that LINC01574 was markedly elevated in BC tissues and cells and was an independent prognostic risk factor for patients with BC. Further functional studies revealed that knockdown of LINC01574 remarkably inhibited the growth and metastasis of BC cells in vitro and in vivo. Mechanistically, LINC01574 competitively binds with miR-6745 to prevent the degradation of TTYH3, thereby promoting the development of BC.
CONCLUSION
Our results unmasked a novel LINC01574/miR-6745/TTYH3 regulatory axis in BC progression and suggested that LINC01574 might be a promising prognostic indicator and therapeutic target for patients with BC.
目的
大量证据表明 lncRNA 在乳腺癌（BC）的发展中发挥着重要作用。本研究旨在挖掘 LINC01574 在 BC 中的功能作用，并进一步挖掘其潜在的调控机制。
方法
通过数据挖掘、生物信息学和 RT-qPCR 的综合分析，检测 LINC01574 在 BC 中的表达和预后。然后，在体外和体内评估 LINC01574 敲低对 BC 细胞生长和转移的影响。通过靶标预测和双荧光素酶报告基因检测揭示 miR-6745 与 LINC01574 或 TTYH3 之间的相互作用。
结果
我们的数据发现，LINC01574 在 BC 组织和细胞中明显上调，是 BC 患者的独立预后危险因素。进一步的功能研究表明，敲低 LINC01574 可显著抑制 BC 细胞在体外和体内的生长和转移。机制上，LINC01574 竞争性结合 miR-6745 以防止 TTYH3 的降解，从而促进 BC 的发展。
结论
我们的研究结果揭示了 BC 进展中一种新的 LINC01574/miR-6745/TTYH3 调控轴，并表明 LINC01574 可能是 BC 患者有前途的预后指标和治疗靶点。
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