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MicroRNA-21 regulates the proliferation and apoptosis of cervical cancer cells via tumor necrosis factor-α

The proliferation and apoptosis of tumor cells are regulated by a variety of microRNAs (miRs). miR-21 can inhibit the apoptosis of cancer cells in vitro. Tumor necrosis factor α (TNF-α) serves an important role in the induction of proliferation of cervical cancer cells. Previous studies have demonst...

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Detalles Bibliográficos
Autores principales: Xu, Lin, Xu, Qian, Li, Xiwen, Zhang, Xiaoling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5647022/
https://www.ncbi.nlm.nih.gov/pubmed/28765959
http://dx.doi.org/10.3892/mmr.2017.7143
Descripción
Sumario:The proliferation and apoptosis of tumor cells are regulated by a variety of microRNAs (miRs). miR-21 can inhibit the apoptosis of cancer cells in vitro. Tumor necrosis factor α (TNF-α) serves an important role in the induction of proliferation of cervical cancer cells. Previous studies have demonstrated that the expression level of miR-21 is associated with TNF-α expression in alveolar macrophages. However, to the best of our knowledge, whether miR-21 regulates TNF-α in cervical cells has not been reported. The present study was designed to investigate whether miR-21 regulates TNF-α expression, proliferation and apoptosis of cervical cancer cells. miR-21, miR-21 inhibitor and control miRNA were synthesized and transfected into HeLa cervical cancer cells. Reverse transcription-quantitative polymerase chain reaction was used to measure the expression levels of miR-21 and TNF-α at the mRNA level. Western blotting was used to measure the expression levels of TNF-α at the protein level. MTT assay and Hoechest-33342 staining were used to measure the proliferation and apoptosis of HeLa cells. miR-21 was identified to upregulate the mRNA and protein expression levels of TNF-α. Furthermore, upregulation of TNF-α enhanced the proliferation capability of HeLa cells. Changes in the expression levels of miR-21 and TNF-α did not significantly affect the apoptosis of Hela cells. In conclusion, the present study demonstrated that miR-21 regulates the expression of TNF-α in HeLa cells. Additionally, the expression level of TNF-α was positively associated with the proliferation capability of Hela cells, but not apoptosis. Therefore, miR-21 regulates the proliferation of HeLa cells through regulation of TNF-α. These results provide novel potential therapeutic targets for the treatment of cervical cancer.