Department of Otolaryngology, Second Affiliated Hospital of Army Medical University, Chongqing, China.
J Biol Regul Homeost Agents. 2019 Mar-Apr;33(2):321-330.
Nasopharyngeal carcinoma (NPC) is a malignant tumor with high invasive and metastatic properties. Dysregulation of miRNAs may contribute to disease progression by targeting disease-related genes. In this study we aimed to elucidate the role and function of aberrantly expressed miRNA in NPC tumorigenesis. We found that miR-1178-3p was highly expressed in NPC tissues. Overexpression of miR-1178-3p promoted the proliferation, migration and invasion of NPC cells in vitro. In contrast, knocking down endogenous miR-1178-3p by miRNA-specific inhibitor significantly suppressed the above phenotypes. Moreover, miR- 1178-3p was shown to negatively regulate serine/threonine-protein kinase 4 (STK4), an NPC-related tumor suppressor gene, in the post-transcriptional level. Furthermore, STK4 overexpression abolished miR-1178- 3p-induced cell proliferation, migration and invasion through STK4-mediated dephosphorylation of AKT. Our results indicate that miR-1178-3p acts as an oncomiRNA in NPC by suppressing STK4 expression, and inhibition of miR-1178-3p may become a therapeutic potential for NPC.
鼻咽癌（NPC）是一种具有高侵袭性和转移性的恶性肿瘤。miRNA 的失调可能通过靶向疾病相关基因导致疾病的进展。在本研究中，我们旨在阐明异常表达的 miRNA 在 NPC 肿瘤发生中的作用和功能。我们发现 miR-1178-3p 在 NPC 组织中高表达。miR-1178-3p 的过表达促进 NPC 细胞在体外的增殖、迁移和侵袭。相比之下，miRNA 特异性抑制剂下调内源性 miR-1178-3p 则显著抑制上述表型。此外，miR-1178-3p 被证明可在转录后水平负调控丝氨酸/苏氨酸蛋白激酶 4（STK4），一种与 NPC 相关的肿瘤抑制基因。此外，通过 STK4 介导的 AKT 去磷酸化，STK4 的过表达可消除 miR-1178-3p 诱导的细胞增殖、迁移和侵袭。我们的研究结果表明，miR-1178-3p 通过抑制 STK4 表达在 NPC 中发挥致癌 miRNA 的作用，抑制 miR-1178-3p 可能成为 NPC 的一种治疗潜力。
