We explored the role and mechanism of miR-214 involvement in the progression of diffuse large B-cell lymphoma (DLBCL). The expression levels of miR-214 and PD-L1 in human DLBCL cell lines and in tissue samples from patients with DLBCL were determined using quantitative RT-PCR. The dual-luciferase reporter assay was employed to determine the correlation between the expressions of miR-214 and PD-L1. Cell viability, invasiveness and apoptosis were respectively examined in cells of the DLBCL line OCI-Ly3 using CCK-8, transwell and flow cytometry assays. The expression level of PD-L1 was determined via immunoblotting. Inflammatory cytokine secretion was determined via enzyme-linked immune sorbent assay (ELISA). miR-214 was downregulated and PD-L1 was upregulated in DLBCL tissues and cell lines in comparison to normal adjacent tissues or normal B-cell. This indicates a negative correlation in the expression levels. Overexpression of miR-214 inhibited cell viability and invasion and induced apoptosis of OCI-Ly3 cells. Moreover, miR-214 was shown to target PD-L1 mRNA by binding to its 3′-untranslated region (UTR). Knockdown of PD-L1 attenuated the malignant phenotype of OCI-Ly3 cells. Overexpression of miR-214 inhibited tumor growth by targeting PD-L1 in vivo. By targeting PD-L1, miR-214 regulates the progression of DLBCL in vitro and in vivo.

中文翻译：

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MiR-214 通过靶向 PD-L1 来阻止弥漫性大 B 细胞淋巴瘤的进展。

我们探讨了 miR-214 在弥漫性大 B 细胞淋巴瘤 (DLBCL) 进展中的作用和机制。使用定量 RT-PCR 测定人类 DLBCL 细胞系和 DLBCL 患者组织样本中 miR-214 和 PD-L1 的表达水平。采用双荧光素酶报告基因测定来确定 miR-214 和 PD-L1 表达之间的相关性。使用 CCK-8、transwell 和流式细胞术分别检测 DLBCL 系 OCI-Ly3 细胞中的细胞活力、侵袭性和细胞凋亡。通过免疫印迹测定PD-L1的表达水平。通过酶联免疫吸附试验（ELISA）测定炎症细胞因子的分泌。与正常邻近组织或正常 B 细胞相比，在 DLBCL 组织和细胞系中 miR-214 下调，PD-L1 上调。这表明表达水平呈负相关。miR-214的过表达抑制细胞活力和侵袭并诱导OCI-Ly3细胞凋亡。此外，显示 miR-214 通过与其 3'-非翻译区 (UTR) 结合来靶向 PD-L1 mRNA。PD-L1 的敲低减弱了 OCI-Ly3 细胞的恶性表型。miR-214 的过表达通过在体内靶向 PD-L1 来抑制肿瘤生长。通过靶向 PD-L1，miR-214 在体外和体内调节 DLBCL 的进展。miR-214 的过表达通过在体内靶向 PD-L1 来抑制肿瘤生长。通过靶向 PD-L1，miR-214 在体外和体内调节 DLBCL 的进展。miR-214 的过表达通过在体内靶向 PD-L1 来抑制肿瘤生长。通过靶向 PD-L1，miR-214 在体外和体内调节 DLBCL 的进展。