The role of microRNA-146b on proliferation and apoptosis of thyroid carcinoma
Xin Qu, Xu Di, Jiaxin Wang, Haichao Zhang, Caixia Li
Abstract
Xin Qu, Xu Di, Jiaxin Wang, Haichao Zhang, Caixia Li
Abstract
Objective To explore the role of microRNA (miRNA, miR)-146b on proliferation and apoptosis of thyroid carcinoma. Methods After miR-146b inhibitor and miR-146b NC were transfected into SW579 cell by liposome LipofectamineTM3000, the expression of miR-146b, cell viability, cell apoptotic rate, cell cycle, the expression of B cell lymphoma/lewkmia-2 (bcl-2), bcl-2 related X protein (bax), cyclin dependent kinases (CDK4), phosphorylation of nuclear factor kappa B (NF-κB) p65 was detected. Results The expression of miR-146b in miR-146b inhibitor group (0.38±0.05) was lower than that in miR-146b NC (1.00±0.09) (P<0.05). Cell viability in miR-146b inhibitor group (0.36±0.04) was lower than that in miR-146b NC group (0.59±0.06) (P<0.05). Cell apoptosis rate (34.58±3.50)% was higher than that in miR-146b NC group (4.28±0.43)% (P<0.05). The cell cycle in miR-146b inhibitor group (44.32±4.43)% was longer than miR-146b NC group (34.08±3.42)% (P<0.05). The expression of bcl-2, Cyclin D1 and CDK4, phosphorylation of NF-κB p65 in miR-146b inhibitor group was lower than that in miR-146b NC group (P<0.05), the expression of bax in miR-146b inhibitor group was higher than that in miR-146b NC group (P<0.05). Conclusion MiR-146b inhibitor might inhibit the proliferation of SW579 cell and induce cell apoptosis via blocking NF-κB signaling pathway. Key words: MicroRNA-146b; Thyroid carcinoma; Proliferation; Apoptosis
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Objective To explore the role of microRNA (miRNA, miR)-146b on proliferation and apoptosis of thyroid carcinoma. Methods After miR-146b inhibitor and miR-146b NC were transfected into SW579 cell by liposome LipofectamineTM3000, the expression of miR-146b, cell viability, cell apoptotic rate, cell cycle, the expression of B cell lymphoma/lewkmia-2 (bcl-2), bcl-2 related X protein (bax), cyclin dependent kinases (CDK4), phosphorylation of nuclear factor kappa B (NF-κB) p65 was detected. Results The expression of miR-146b in miR-146b inhibitor group (0.38±0.05) was lower than that in miR-146b NC (1.00±0.09) (P<0.05). Cell viability in miR-146b inhibitor group (0.36±0.04) was lower than that in miR-146b NC group (0.59±0.06) (P<0.05). Cell apoptosis rate (34.58±3.50)% was higher than that in miR-146b NC group (4.28±0.43)% (P<0.05). The cell cycle in miR-146b inhibitor group (44.32±4.43)% was longer than miR-146b NC group (34.08±3.42)% (P<0.05). The expression of bcl-2, Cyclin D1 and CDK4, phosphorylation of NF-κB p65 in miR-146b inhibitor group was lower than that in miR-146b NC group (P<0.05), the expression of bax in miR-146b inhibitor group was higher than that in miR-146b NC group (P<0.05). Conclusion MiR-146b inhibitor might inhibit the proliferation of SW579 cell and induce cell apoptosis via blocking NF-κB signaling pathway. Key words: MicroRNA-146b; Thyroid carcinoma; Proliferation; Apoptosis
Key concepts: Apoptosis, microRNA, Cyclin D1, Cell growth, Cell cycle, Viability assay, Cancer research, Kinase