LINC01857 has been proven to be involved in glioma and breast cancer. However, the biological function of LINC01857 in diffuse large B-cell lymphoma (DLBCL) is poorly investigated. By accessing to the Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTE_X), LINC01857 expression was found upregulated in both DLBCL tissues and cells. Cell proliferation and flow cytometry assays showed that LINC01857 promoted proliferation and cell cycle, but suppressed apoptosis in DLBCL cells. Bioinformatics analysis and luciferase reporter assay confirmed that LINC01857 may serve as a sponge for miR-141-3p and miR-141-3p may target MAP4K4. Mechanically, the regulatory action of miR-141-3p/MAP4K4 on DLBCL cellular behaviors was regulated by LINC01857. In addition, LINC01857 could increase the activity of PI3K/mTOR pathway and facilitate the EMT process in a miR-141-3p-mediated manner in DLBCL. Our data illustrated that the LINC01857/miR-141-3p/MAP4K4 might function as a promising therapeutic avenue for DLBCL treatment.

LINC01857 已被证明与神经胶质瘤和乳腺癌有关。然而，LINC01857 在弥漫性大 B 细胞淋巴瘤 (DLBCL) 中的生物学功能研究很少。通过访问癌症基因组图谱 (TCGA) 和基因型组织表达 (GTE _X), LINC01857 表达在 DLBCL 组织和细胞中均被上调。细胞增殖和流式细胞术分析表明，LINC01857 促进增殖和细胞周期，但抑制 DLBCL 细胞凋亡。生物信息学分析和荧光素酶报告基因分析证实，LINC01857 可作为 miR-141-3p 的海绵，miR-141-3p 可靶向 MAP4K4。从机械上讲，miR-141-3p/MAP4K4 对 DLBCL 细胞行为的调节作用受 LINC01857 调节。此外，LINC01857 可以增加 PI3K/mTOR 通路的活性，并以 miR-141-3p 介导的方式促进 DLBCL 中的 EMT 过程。我们的数据表明 LINC01857/miR-141-3p/MAP4K4 可能作为 DLBCL 治疗的有前途的治疗途径。