MicroRNA (miR) plays a critical role in the progression of multiple malignancies. Nevertheless, knowledge of the role it plays in laryngeal cancer is limited. In this study, we explored the role of miR-892a in laryngeal cancer cell proliferation and apoptosis. miR-892a expression was increased in 17 laryngeal cancer samples and cells compared with that in healthy tissues, laryngeal cancer normal surrounding tissues, and the NP69 human nasopharyngeal epithelial cell line. Conversely, Dicer expression was downregulated in human laryngeal cancer samples as well as in the laryngeal cancer cell lines. CCK-8 assays and colony formation assay confirmed that depleted miR-892a expression damaged the proliferation and growth of TU212 and M4E cells. Annexin V/PI flow cytometry displayed that miR-892a inhibition led to increased apoptosis of TU212 and M4E cells. By conducting bioinformatic analysis and dual-luciferase reporter assay, it was revealed that that miR-892a targets Dicer 3′-UTR for silencing. Dicer expression inhibition offsets the effect of miR-892a on the growth and apoptosis of laryngeal cancer cells. Dicer overexpression displayed similar phenotype with miR-892a inhibition on the properties of laryngeal cancer cells. Results of in vivo experiments further confirmed that miR-892a silencing suppressed tumor growth in a mouse model. Hence, the results of this study provide new ideas about the biological and molecular mechanisms behind laryngeal cancer progression, thereby obtaining novel laryngeal cancer treatments.

Impact statement

This work expanded the knowledge of the molecular mechanisms underlying LC progression by exploring the role of miR-892a in the viability of TU212 and M4E cells. The results showed that miR-892a, which exhibited elevated expression in LC cells and tissue specimens of patients with LC, exerted an inhibitory effect on Dicer expression, whereas silencing of miR-892a in TU212 and M4E cells hindered cell proliferation and growth and promoted apoptosis. Furthermore, miR-892a was demonstrated to directly target Dicer 3′-UTR and inhibit its expression. These findings demonstrated that miR-892a acted as an LC oncogene via its action on Dicer, which further confirmed that miR-892a can serve as a diagnostic indicator or promising agent for LC treatment.

中文翻译：

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MicroRNA-892a 通过 Dicer 调节喉癌细胞增殖。

MicroRNA (miR) 在多种恶性肿瘤的进展中起着关键作用。然而，关于它在喉癌中所起的作用的知识是有限的。在本研究中，我们探讨了 miR-892a 在喉癌细胞增殖和凋亡中的作用。与健康组织、喉癌正常周围组织和 NP69 人鼻咽上皮细胞系相比，17 个喉癌样本和细胞中 miR-892a 的表达增加。相反，Dicer 表达在人喉癌样本以及喉癌细胞系中被下调。CCK-8 测定和集落形成测定证实，miR-892a 表达的缺失损害了 TU212 和 M4E 细胞的增殖和生长。膜联蛋白 V/PI 流式细胞术显示 miR-892a 抑制导致 TU212 和 M4E 细胞凋亡增加。通过进行生物信息学分析和双荧光素酶报告基因检测，发现 miR-892a 靶向 Dicer 3'-UTR 进行沉默。Dicer 表达抑制抵消了 miR-892a 对喉癌细胞生长和凋亡的影响。Dicer 过表达显示出与 miR-892a 抑制喉癌细胞特性相似的表型。结果 Dicer 过表达显示出与 miR-892a 抑制喉癌细胞特性相似的表型。结果 Dicer 过表达显示出与 miR-892a 抑制喉癌细胞特性相似的表型。结果体内实验进一步证实，miR-892a 沉默抑制了小鼠模型中的肿瘤生长。因此，本研究的结果为喉癌进展背后的生物学和分子机制提供了新的思路，从而获得了新的喉癌治疗方法。

影响陈述

这项工作通过探索 miR-892a 在 TU212 和 M4E 细胞活力中的作用，扩展了对 LC 进展的分子机制的认识。结果表明miR-892a在LC细胞和LC患者组织标本中表达升高，对Dicer表达有抑制作用，而TU212和M4E细胞中miR-892a的沉默阻碍细胞增殖和生长，促进细胞凋亡. 此外，miR-892a 被证明可以直接靶向 Dicer 3'-UTR 并抑制其表达。这些发现表明 miR-892a 通过其对 Dicer 的作用而充当 LC 致癌基因，这进一步证实了 miR-892a 可以作为 LC 治疗的诊断指标或有希望的药物。