Laryngeal papillomas (LP) is a difficult disease to manage due to its frequent recurrence, airway compromise, and risk of cancer. Recently, growing evidence indicates the aberrant expression of OGFPD1, a stress granule protein, links closely to the development of tumorigenesis; however, little is known about its role in LP progression. Here, we investigated the tumor promoting action of OGFOD1 in LP. The transcriptional and translational levels of OGFOD1 were significantly up-regulated in LP tissues and cells. Moreover, OGFOD1 promoted viability and proliferation, and inhibited LP cells apoptosis. We further revealed that OGFOD1 was directly targeted by miR-1224-5p, which was significantly down-regulated in LP. Overexpression of the miR-1224-5p suppressed OGFOD1-induced cell proliferation and viability, and promoted apoptosis of LP. In accordance, knockdown of miR-1224-5p inversed the inhibitory effects. In confederation of the central involvement of OGFOD1 in LP progression, targeting the miR-1224-5p/OGFOD1 pathway might provide a novel strategy for LP treatment.

中文翻译：

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由miR-1224-5p负调控的OGFOD1促进人乳头瘤病毒感染的喉乳头状瘤的增殖。

喉乳头状瘤（LP）由于其频繁复发，气道受损和患癌风险而难以治疗。最近，越来越多的证据表明，应激颗粒蛋白OGFPD1的异常表达与肿瘤发生的发展密切相关。然而，对其在LP进展中的作用了解甚少。在这里，我们调查了LP中OGFOD1的肿瘤促进作用。在LP组织和细胞中，OGFOD1的转录和翻译水平显着上调。此外，OGFOD1促进活力和增殖，并抑制LP细胞凋亡。我们进一步揭示OGFOD1直接被miR-1224-5p靶向，而后者在LP中显着下调。miR-1224-5p的过表达抑制了OGFOD1诱导的细胞增殖和活力，并促进了LP的凋亡。按照，敲低miR-1224-5p可逆转抑制作用。在OGFOD1参与LP进展的重要过程中，靶向miR-1224-5p / OGFOD1途径可能为LP治疗提供一种新策略。