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Merck

MicroRNA-152 suppresses cisplatin resistance in A549 cells.

Oncology letters (2019-10-16)
Wenfei Zhao, Hongyun Li, Shanshan Yang, Di Guo, Jing Chen, Shaoyi Miao, Yi Xin, Miaomiao Liang
摘要

The present study aimed to investigate the association between microRNA-152 and cisplatin resistance in non-small cell lung cancer. A549 and cisplatin-resistant A549 cells (A549/cis) were maintained in vitro. Reverse transcription-quantitative PCR (RT-qPCR) was performed to analyze differences in microRNA-152 levels between A549 and A549/cis cells, and changes in Bcl-2 and NF-κB expression levels were analyzed via RT-qPCR and western blot analyses. MicroRNA-152 was overexpressed in A549/cis cells via transfection of a microRNA-152 mimic. Upon treating transfected or untransfected A549/cis cells with 2 µg/l cisplatin for 24 h, a Cell Counting Kit-8 assay, morphological analysis and flow cytometry analysis were performed to evaluate the effect of microRNA-152 on the inhibition of cell proliferation and induction of apoptosis. Furthermore, changes in Bcl-2 and NF-κB expression levels in microRNA-152-overexpressing A549/cis cells were also analyzed. MicroRNA-152 was significantly downregulated and Bcl-2 and NF-κB were significantly upregulated in A549/cis cells (P<0.05). MicroRNA-152 upregulation enhanced the inhibitory effect of cisplatin on A549/cis cells. These results suggest that microRNA-152 downregulates Bcl-2 and NF-κB. MicroRNA-152 downregulation may induce cisplatin resistance in non-small cell lung cancer cells, whereas microRNA-152 upregulation may improve cisplatin sensitivity among A549/cis cells via downregulation of Bcl-2 and NF-κB.

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单克隆抗 GAPDH-过氧物酶 小鼠抗, clone GAPDH-71.1, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
Monoclonal Anti-NF-κB antibody produced in mouse, clone NF-12, ascites fluid