MiR-16-1 Targeted Silences Far Upstream Element Binding Protein 1 to Advance the Chemosensitivity to Adriamycin in Gastric Cancer
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Chemotherapy can prevent metastasis and recurrence of gastric cancer (GC), and is a well supplement for operation. But, chemotherapy resistance has severely restricted the application of chemotherapy. This study aimed to investigate the regulatory roles and molecular mechanism of miR-16-1 to the chemosensitivity to adriamycin in GC. In this study, the expression of miR-16-1 and FUBP1 was down-regulated and up-regulated respectively in adriamycin-resistant GC tissues and cell lines, and represented a negative relationship between them. MiR-16-1 could silence FUBP1 directly and specifically, FUBP1 was a target gene of miR-16-1. Silence of FUBP1 inhibited the half maximal inhibitory concentration (IC50) of SGC7901/AR cell line to adriamycin, chemosensitivity enhanced significantly. Moreover, FUBP1 silence in SGC7901/AR cell line also inhibited proliferation and invasion, and advanced cell apoptosis. To sum up, the expression of miR-16-1 was positively related with the chemosensitivity of GC to adriamycin, and miR-16-1 could targeted silence FUBP1 to advance the chemosensitivity to adriamycin in GC, which might be a novel potential therapeutic target for GC.
KeywordsGastric cancer microRNA-16-1 Far upstream element binding protein 1 Chemosensitivity Adriamycin
This work was supported by the National Nature Science Foundation of China (81272716).
DZ and LS participated in the study design and drafted the manuscript. DZ and YZ carried out the in vitro studies and performed the statistical analysis. DZ conceived of the study and helped to draft the manuscript. All authors read and approved the final manuscript.
Compliance with Ethical Standards
Conflict of Interest
The authors declare that they have no competing interests.
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