Emerging investigations have demonstrated that lncRNAs are key crucial modulators in cancer. In this study, we investigated the role of LINC02381 in breast cancer (BC). Reverse transcriptase quantitative polymerase chain reaction measured the LINC02381 level in BC tissues and cells. Colony formation, EdU staining, wound healing and Transwell experiments examined the impact of LINC02381 depletion on BC cell phenotypes. Relationship among miR-1271-5p, LINC02381, and FN1 was tested through applying RIP, luciferase reporter, and RNA pull-down assays. We found that LINC02381 expression was elevated in BC. Functionally, LINC02381 knockdown hampered BC cell proliferation, migration, and invasion. LINC02381 overexpression accelerated tumor formation in vivo. Mechanistically, LINC02381 acted as a ceRNA to increase FN1 via decoying miR-1271-5p. Additionally, LINC02381 activated PI3K/AKT pathway by upregulating FN1. Rescue assays indicated that FN1 upregulation or PI3K/AKT activation rescued the LINC02381 knockdown-mediated inhibition on malignant phenotypes of BC cells. Overall, LINC02381 exerts carcinogenic effects in BC by the miR-1271-5p/FN1 axis to activate PI3K/AKT pathway.

中文翻译：

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LINC02381通过miR-1271-5p/FN1轴激活PI3K/AKT通路加重乳腺癌

新兴研究表明，lncRNA 是癌症的关键调节剂。在这项研究中，我们调查了 LINC02381 在乳腺癌 (BC) 中的作用。逆转录酶定量聚合酶链反应测量了 BC 组织和细胞中的 LINC02381 水平。集落形成、EdU 染色、伤口愈合和 Transwell 实验检查了 LINC02381 消耗对 BC 细胞表型的影响。miR-1271-5p、LINC02381 和 FN1 之间的关系通过应用 RIP、荧光素酶报告基因和 RNA 下拉分析进行了测试。我们发现在 BC 中 LINC02381 表达升高。在功能上，LINC02381 敲低阻碍了 BC 细胞增殖、迁移和侵袭。LINC02381 过表达加速了体内肿瘤的形成。从机制上讲，LINC02381 作为 ceRNA 通过诱骗 miR-1271-5p 来增加 FN1。此外，LINC02381 通过上调 FN1 激活 PI3K/AKT 通路。拯救分析表明，FN1 上调或 PI3K/AKT 激活拯救了 LINC02381 敲低介导的对 BC 细胞恶性表型的抑制。总体而言，LINC02381 通过 miR-1271-5p/FN1 轴激活 PI3K/AKT 通路在 BC 中发挥致癌作用。