本研究的目的是阐明长链非编码RNA（lncRNA）转移相关肺腺癌转录本1（MALAT1）在宫颈癌细胞焦亡过程中的作用及其下游机制。使用从患者和 U14 宫颈肿瘤裸鼠中分离的原代细胞确定了抑制 lncRNA MALAT1 对宫颈癌细胞的作用。确定 lncRNA MALAT1 表达水平和细胞活力以进行关系分析。然后在经过或不经过脂多糖 (LPS) 处理的 lncRNA MALAT1 敲低或过表达的 HeLa 细胞中研究细胞焦亡。利用生物信息学工具识别lncRNA MALAT1的下游因子，随后通过宫颈癌细胞焦亡过程中的功能获得或丧失分析进行验证。结果发现，与癌旁细胞相比，lncRNA MALAT1在宫颈癌细胞中的表达水平显着升高，并且lncRNA MALAT1的敲低可诱导宫颈癌细胞通过细胞焦亡而死亡。相比之下，lncRNA MALAT1 的过度表达可阻断 LPS 诱导的细胞焦亡。这些结果与生物信息学统计工具相结合，证明 microRNA (miR)-124/sirtuin 1 (SIRT1) 轴可能至少部分通过介导 lncRNA MALAT1 对宫颈癌细胞焦亡的影响来影响宫颈癌的进展。总之，宫颈癌细胞中的lncRNA MALAT1/miR-124/SIRT1调节轴可能介导细胞焦亡，并可能提供对抗宫颈癌进展的潜在靶点。

The aim of the present study was to elucidate the role and downstream mechanism of long non‑coding RNA (lncRNA) metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1) in the process of cervical cancer cell pyroptosis. The effect of inhibiting lncRNA MALAT1 on cervical cancer cells was determined using primary cells isolated from patients and U14 cervical tumor‑bearing nude mice. The level of lncRNA MALAT1 expression and cell viability were determined for relationship analysis. Pyroptosis was then investigated in HeLa cells with lncRNA MALAT1 knockdown or overexpression with or without lipopolysaccharide (LPS) treatment. Bioinformatics tools were used to identify downstream factors of lncRNA MALAT1, which were subsequently verified by gain‑ or loss‑of‑function analyses in the process of cervical cancer cell pyroptosis. It was observed that the level of lncRNA MALAT1 was markedly higher in cervical carcinoma cells compared with expression in paracarcinoma cells, and knockdown of lncRNA MALAT1 induced cervical cancer cell death through pyroptosis. By contrast, overexpression of lncRNA MALAT1 blocked LPS‑induced pyroptosis. These results, combined with bioinformatics statistical tools, demonstrated that the microRNA (miR)‑124/sirtuin 1 (SIRT1) axis may affect the progression of cervical cancer at least partly by mediating the effect of lncRNA MALAT1 on the pyroptosis of cervical cancer cells. In conclusion, the lncRNA MALAT1/miR‑124/SIRT1 regulatory axis in cervical cancer cells may mediate pyroptosis and may provide potential targets against the progression of cervical cancer.