European review for medical and pharmacological sciences · 2019
MicroRNA-23a inhibits the growth of papillary thyroid carcinoma via regulating cyclin G1.
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Yin J-J, Cheng X-Y
Аннотация
OBJECTIVE: The aim of this study was to investigate the regulatory mechanism of miR-23a on biological behaviors of papillary thyroid carcinoma (PTC) cells, such as cell proliferation, cell cycle and apoptosis.
PATIENTS AND METHODS: The expression of miR-23a in 28 paired of PTC tissue samples and matched adjacent tissues was detected by quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Meanwhile, miR-23a expression in PTC cell lines was also detected by qRT-PCR. Subsequently, miR-23a mimics and inhibitor were transfected into PTC cells. The effects of gain or loss of miR-23a on cell proliferation, cell cycle and apoptosis were analyzed. Bioinformatics analysis, Dual-Luciferase activity assay and Western blot were recruited to validate the potential target gene of miR-23a.
RESULTS: The expression of miR-23a was significantly decreased in PTC tissue samples and cell lines. Upregulation of miR-23a in PTC cells markedly decreased cell proliferation, induced cell cycle arrest at G0/G1 phase and promoted cell apoptosis. However, decreased miR-23a exerted the opposite effects. Dual-Luciferase, qRT-PCR and Western blot showed that CCNG1 was a target gene of miR-23a. Furthermore, the silence of CCNG1 intensified the suppressive effect of miR-23a on cell growth.
CONCLUSIONS: MiR-23a was involved in the development of PTC via targeting CCNG1, which might provide a new prospect for PTC diagnosis and therapy.
PATIENTS AND METHODS: The expression of miR-23a in 28 paired of PTC tissue samples and matched adjacent tissues was detected by quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). Meanwhile, miR-23a expression in PTC cell lines was also detected by qRT-PCR. Subsequently, miR-23a mimics and inhibitor were transfected into PTC cells. The effects of gain or loss of miR-23a on cell proliferation, cell cycle and apoptosis were analyzed. Bioinformatics analysis, Dual-Luciferase activity assay and Western blot were recruited to validate the potential target gene of miR-23a.
RESULTS: The expression of miR-23a was significantly decreased in PTC tissue samples and cell lines. Upregulation of miR-23a in PTC cells markedly decreased cell proliferation, induced cell cycle arrest at G0/G1 phase and promoted cell apoptosis. However, decreased miR-23a exerted the opposite effects. Dual-Luciferase, qRT-PCR and Western blot showed that CCNG1 was a target gene of miR-23a. Furthermore, the silence of CCNG1 intensified the suppressive effect of miR-23a on cell growth.
CONCLUSIONS: MiR-23a was involved in the development of PTC via targeting CCNG1, which might provide a new prospect for PTC diagnosis and therapy.