LncRNA NR2F1-AS1 inhibits the malignant properties of cervical cancer cells via targeting miR-642a-3p/NR2F1 axis

• Lingyan Zhang ^[1] ; Yanhua Zhang ^[1] ; Jianbo Zhou ^[1] ; Yongfang Wang ; Haihong Wang ^[1] ; Mei Huang ^[1] ; Qiulan Yu ^[1] ; Qi Sun ^[1]
  1. [1] Department of Obstetrics and Gynecology, Binhai County People’s Hospital, Jiangsu, China
• Localización: Revista de investigación clínica, ISSN 0034-8376, ISSN-e 2564-8896, Vol. 74, Nº. 4, 2022, págs. 181-192
• Idioma: inglés
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• Resumen

  • Background: Cervical cancer (CC), as a serious menace to the health of women, has long been one of the most lethal gynecologic neoplasms throughout the world. Long non-coding RNA (LncRNA) NR2F1-AS1 has been documented to exert crucial functions in many malignant tumors. Nonetheless, the function and molecular mechanism of NR2F1-AS1 in CC remain completely unknown. Objective: This study aimed to explore the function and molecular mechanism of NR2F1-AS1 in CC. Methods: The expression levels of NR2F1-AS1, miR-642a-3p, NR2F1 in CC tissues, and cell lines were examined by reverse transcription real-time quantitative polymerase chain reaction. Cell viability, proliferation, migration, and invasion were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide, colony formation and Transwell assays. The protein levels of epithelial-mesenchymal transition markers and NR2F1 in CC cells were assessed by Western blot analysis. The correlations among NR2F1-AS1, miR-642a-3p, and NR2F1 were estimated through luciferase reporter and RNA immunoprecipitation assays. Results: NR2F1-AS1 expression was clearly downregulated in CC tissues and cell lines. Molecular mechanistic experiments showed that NR2F1-AS1 overexpression upregulated NR2F1 expression in CC cells by directly binding to miR-642a-3p, and inhibiting by this way cell viability, proliferation, migration, and invasion in CC. Rescue assays showed that NR2F1 knockdown or miR-642a-3p overexpression offset NR2F1-AS1 upregulation-induced inhibition on CC cell malignant phenotypes. Conclusion: These findings revealed that NR2F1-AS1 played a tumor suppressor role in CC by mediating the miR-642a-3p/NR2F1 axis.