Knockdown of lncRNA <i>MALAT1</i> induces pyroptosis by regulating the miR‑124/SIRT1 axis in cervical cancer cells
Tian Liang, Tong Lü, Weiwei Jia, R. Li, Min Jiang, Jiao Yu, Yuchen Wang, Shanshan Cong, Xinyan Jiang, Lina Dong, Yingyu Zhou, Guangmei Zhang, Dan Xiao
Abstract
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 (<em>MALAT1</em>) in the process of cervical cancer cell pyroptosis. The effect of inhibiting lncRNA <em>MALAT1</em> on cervical cancer cells was determined using primary cells isolated from patients and U14 cervical tumor‑bearing nude mice. The level of lncRNA <em>MALAT1</em> expression and cell viability were determined for relationship analysis. Pyroptosis was then investigated in HeLa cells with lncRNA <em>MALAT1</em> knockdown or overexpression with or without lipopolysaccharide (LPS) treatment. Bioinformatics tools were used to identify downstream factors of lncRNA <em>MALAT1</em>, 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 <em>MALAT1</em> was markedly higher in cervical carcinoma cells compared with expression in paracarcinoma cells, and knockdown of lncRNA <em>MALAT1</em> induced cervical cancer cell death through pyroptosis. By contrast, overexpression of lncRNA <em>MALAT1</em> 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 <em>MALAT1</em> on the pyroptosis of cervical cancer cells. In conclusion, the lncRNA <em>MALAT1</em>/miR‑124/SIRT1 regulatory axis in cervical cancer cells may mediate pyroptosis and may provide potential targets against the progression of cervical cancer.