The cancer-promoting function of the long non-coding RNA (lncRNA) LPP-AS2 has been documented in different cancers. Nonetheless, its role in thyroid carcinoma (THCA) remains unestablished. Reverse transcription quantitative polymerase chain reaction and Western blotting were conducted to estimate the expressions of lncRNA LPP-AS2, miR-132-3p, and OLFM1. The THCA cells' functions were assessed through CCK8 assays, Transwell invasion assays, scratch wound-healing migration assays, and quantification of caspase-3 activity. The in vivo assays were also implemented to assess tumor growth. Luciferase reporter and RNA immuno-precipitation assay (RIPA) experiments were executed to elucidate the interactions of miR-132-3p with lncRNA LPP-AS2 and OLFM1. THCA tissues and cells exhibited poor lncRNA LPP-AS2 and OLFM1 expressions and a robust expression of miR-132-3p. Overexpressing lncRNA LPP-AS2 constrained THCA cell proliferation, migration, and invasion and improved caspase-3 activity. The anti-tumor function of lncRNA LPP-AS2 was also validated in vivo. miR-132-3p had an interplay with lncRNA LPP-AS2 and OLFM1. Functionally, overexpressing miR-132-3p promoted the malignant THCA cell phenotypes. However, that tumor promotion was abolished by the additional overexpression of lncRNA LPP-AS2. The in vitro experiments also demonstrated that the repressive effect of OLFM1 overexpression on THCA cell malignant action could be offset by the miR-132-3p mimic. lncRNA LPP-AS2 impedes THCA progression via the miR-132-3p/OLFM1 axis. Our findings contribute a potential strategy in interfering with THCA progression.

中文翻译：

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长链非编码 RNA LPP-AS2 通过调节 miR-132-3p/OLFM1 轴在甲状腺癌中发挥抗肿瘤作用

长链非编码 RNA (lncRNA) LPP-AS2 的促癌功能已在不同的癌症中得到证实。尽管如此，它在甲状腺癌 (THCA) 中的作用仍未确定。进行逆转录定量聚合酶链反应和Western blotting以估计lncRNA LPP-AS2、miR-132-3p和OLFM1的表达。THCA 细胞的功能通过 CCK8 测定、Transwell 侵袭测定、划痕伤口愈合迁移测定和 caspase-3 活性定量进行评估。还实施了体内测定以评估肿瘤生长。执行荧光素酶报告基因和 RNA 免疫沉淀测定 (RIPA) 实验以阐明 miR-132-3p 与 lncRNA LPP-AS2 和 OLFM1 的相互作用。THCA 组织和细胞表现出较差的 lncRNA LPP-AS2 和 OLFM1 表达以及 miR-132-3p 的强表达。过表达 lncRNA LPP-AS2 限制了 THCA 细胞的增殖、迁移和侵袭，并提高了 caspase-3 的活性。lncRNA LPP-AS2的抗肿瘤功能也得到验证体内。miR-132-3p 与 lncRNA LPP-AS2 和 OLFM1 相互作用。在功能上，过表达 miR-132-3p 促进恶性 THCA 细胞表型。然而，lncRNA LPP-AS2 的额外过表达消除了肿瘤促进作用。体外实验还表明，OLFM1 过表达对 THCA 细胞恶性作用的抑制作用可以被 miR-132-3p 模拟物抵消。lncRNA LPP-AS2 通过 miR-132-3p/OLFM1 轴阻碍 THCA 进展。我们的研究结果为干扰 THCA 进展提供了一种潜在策略。