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MiR-218 increases sensitivity to cisplatin in esophageal cancer cells via targeting survivin expression

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Abstract Objectives Increasing evidence showed that microRNAs (miRNAs) were implicated in the chemical resistance of human cancers. We intended to investigate the role of miR-218 in cisplatin sensitivity of esophageal cancer cells. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to analyze miR-218 expression in human esophageal cancer cell line Eca9706 and a cisplatin-resistant subline (ECa9706-CisR cells). The effects of miR-218 transfection on ECa9706 and ECa9706-CisR cell viability, including cell viability and apoptosis rate were confirmed using MTT assay, or flow cytometry, respectively. qRT-PCR was used to validate survivin as a direct target gene of miR-218 in our system. Results We found that miR-218 was significantly decreased in ECa9706-CisR cells compared with parent Eca9706 cells. Overexpression of miR-218 by mimics transfection would enhance cisplatin sensitivity evaluated by cell viability inhibition and apoptosis promotion. We validated here survivin as a direct target of miR-218 in ECa9706 cells, which might contribute to the chemoresistance of esophageal cancer cells to cisplatin. Conclusions In summary, our data suggest that miR-218 might represent as a promising sensitizer of cisplatin therapy in clinical esophageal cancer patients.
Title: MiR-218 increases sensitivity to cisplatin in esophageal cancer cells via targeting survivin expression
Description:
Abstract Objectives Increasing evidence showed that microRNAs (miRNAs) were implicated in the chemical resistance of human cancers.
We intended to investigate the role of miR-218 in cisplatin sensitivity of esophageal cancer cells.
Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to analyze miR-218 expression in human esophageal cancer cell line Eca9706 and a cisplatin-resistant subline (ECa9706-CisR cells).
The effects of miR-218 transfection on ECa9706 and ECa9706-CisR cell viability, including cell viability and apoptosis rate were confirmed using MTT assay, or flow cytometry, respectively.
qRT-PCR was used to validate survivin as a direct target gene of miR-218 in our system.
Results We found that miR-218 was significantly decreased in ECa9706-CisR cells compared with parent Eca9706 cells.
Overexpression of miR-218 by mimics transfection would enhance cisplatin sensitivity evaluated by cell viability inhibition and apoptosis promotion.
We validated here survivin as a direct target of miR-218 in ECa9706 cells, which might contribute to the chemoresistance of esophageal cancer cells to cisplatin.
Conclusions In summary, our data suggest that miR-218 might represent as a promising sensitizer of cisplatin therapy in clinical esophageal cancer patients.

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