Laryngeal squamous cell carcinoma (LSCC) is one of the most common subtypes of head and neck malignancies worldwide. Long intervening/intergenic noncoding RNAs (LINCRNAs) have been recently implicated in various biological processes that take place in the setting of laryngeal cancer, but the regulatory role of LINC00319 in LSCC remains largely unknown. The current study aimed to elucidate the regulatory effect of LINC00319 on the development and progression of LSCC via high-mobility group box 3 (HMGB3). Microarray-based analysis was initially conducted to identify differentially expressed long noncoding RNAs, after which the expression of LINC00319 and HMGB3 in LSCC tissues and cells was determined accordingly. CD133⁺CD144⁺ TU177 cells were subsequently isolated and transfected with LINC00319 overexpression vector (oe-LINC00319), short hairpin RNA (sh)-LINC00319, sh-HMGB3, sh-E2F transcription factor 1 (E2F1), and oe-E2F1, as well as their corresponding controls. The proliferative, invasion, self-renewal, and tumorigenic abilities of CD133⁺CD144⁺ TU177 cells were then evaluated. Our in vitro findings were further confirmed following subcutaneous injection of cells expressing the corresponding plasmids into nude mice. LINC00319 and HMGB3 expressions were elevated in LSCC cells and tissues. LINC00319 increased HMGB3 expression by recruiting E2F1. Furthermore, the stimulatory role of LINC00319 on the proliferation, invasion, self-renewal ability, and tumorigenicity of CD133⁺CD144⁺ TU177 cells was achieved by upregulating HMGB3 via recruitment of E2F1. The in vitro findings were also confirmed by in vivo experiments. Taken together, these data show that downregulating LINC00319 in CD133⁺CD144⁺ TU177 cells may serve as a potential anticancer regimen by inhibiting the proliferation and invasion of cancer stem cells in LSCC.

喉鳞状细胞癌（LSCC）是全球头颈部恶性肿瘤最常见的亚型之一。长干预/基因间非编码 RNA (LINCRNA) 最近与喉癌环境中发生的各种生物学过程有关，但 LINC00319 在 LSCC 中的调节作用仍然很大程度上未知。目前的研究旨在通过高迁移率组框 3 (HMGB3) 阐明 LINC00319 对 LSCC 发展和进展的调节作用。最初进行基于微阵列的分析以鉴定差异表达的长非编码 RNA，然后相应地确定 LINC00319 和 HMGB3 在 LSCC 组织和细胞中的表达。CD133 ⁺ CD144 ⁺随后分离 TU177 细胞并用 LINC00319 过表达载体 (oe-LINC00319)、短发夹 RNA (sh)-LINC00319、sh-HMGB3、sh-E2F 转录因子 1 (E2F1) 和 oe-E2F1 以及它们相应的控制。^{然后评估CD133 +} CD144 ⁺ TU177细胞的增殖、侵袭、自我更新和致瘤能力。在将表达相应质粒的细胞皮下注射到裸鼠中后，我们的体外研究结果得到了进一步证实。LINC00319 和 HMGB3 表达在 LSCC 细胞和组织中升高。LINC00319 通过招募 E2F1 增加了 HMGB3 的表达。^{此外，LINC00319 对 CD133 +} CD144的增殖、侵袭、自我更新能力和致瘤性的刺激作用⁺ TU177 细胞是通过募集 E2F1 上调 HMGB3 实现的。体内实验也证实了体外研究结果。总之，这些数据表明，下调 CD133 ⁺ CD144 ⁺ TU177 细胞中的 LINC00319 可能通过抑制 LSCC 中癌症干细胞的增殖和侵袭而作为一种潜在的抗癌方案。