Abstract

Objective The morbidity and mortality of cervical cancer (CC) rank the fourth-most common among cancers in females, seriously threatening women's health and affecting their quality of life. However, the molecular mechanism of CC development remains poorly understood. This study investigates the role of lncRNA SCIRT in the development of CC. Methods The expression profile of long noncoding RNA stem cell inhibitory RNA transcript (lncRNA SCIRT) in CC (n = 34), tumor-adjacent tissue, and CC cell culture was determined through fluorescence quantitative PCR. The knockdown /overexpressed lncRNA SCIRT vectors were constructed and transfected into cells, and the effects of knockdown or overexpression of lncRNA SCIRT on the proliferative, invasive, and migratory properties of CC cells were determined through Cell Counting Kit-8 (CCK-8), colony forming, and Transwell experiments. Western blot was employed to determine the knockdown/overexpression efficiency of SCIRT and its role on the expression of proteins (e-cadherin, n-cadherin, vimentin, matrix metalloproteinase (MMP)-9 and MMP-2) in CC cells. Finally, SCIRT knockdown on the proliferative ability for CC cells was determined through tumorigenic experiment in nude mice. Results LncRNA SCIRT was highly expressed in CC tissues and cells, and significantly linked with clinical/pathology-based characteristics of patients, including Federation Internationale of Gynecologie and Obstetrigue (FIGO) stage, tumor dimensions, and lymph-node metastasis. SCIRT knockdown markedly reduced CC proliferative, colony forming, and invasive properties, while overexpressing SCIRT promoted the proliferative and invasive properties of CC. Western blotting analysis demonstrated that SCIRT knockdown upregulated e-cadherin and downregulated n-cadherin, vimentin, MMP-9, and MMP-2. Meanwhile, overexpressing SCIRT of lncRNA SCIRT had the opposite effect. Tumorigenic experiment showed that SCIRT knockdown could markedly reduce CC proliferative property the nude mouse. Conclusion LncRNA SCIRT was highly expressed in CC clinical cases. Knockdown/overexpressing SCIRT affected CC proliferative/invasive properties. Hence, lncRNA SCIRT is a promising drug-target and a new biological diagnostic molecule for CC patients.

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