Saudi Journal of Gastroenterology
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ORIGINAL ARTICLE
Year : 2015  |  Volume : 21  |  Issue : 5  |  Page : 313-319

MiR-26a enhances the sensitivity of gastric cancer cells to cisplatin by targeting NRAS and E2F2


1 Department of Gastroenterology, Affiliated Zhuzhou People's Hospital, Changsha Medical University, China
2 Department of Gastroenterology, Shaoxing Central Hospital, Shaoxing, Zhejiang Province, China
3 Intensive Care Unit, the Second Xiangya Hospital, Central South University, Changsha, Hunan Province, China

Correspondence Address:
Dr. Yanyan Zhou
Intensive Care Unit, the Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha 410011, Hunan Province
China
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Source of Support: This work was supported by grant from the Nature Scientific Foundation of China (No. 81101526), Conflict of Interest: None


DOI: 10.4103/1319-3767.166206

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Background/Aims: MiR-26a has been identified as a tumor suppressor in various tumors, but the relationship between miR-26a and the sensitivity of gastric cancer to chemotherapies has not been established. The present study was performed to investigate the effect of miR-26a on drug sensitivity in gastric cancer (GC). Materials and Methods: The expression level of miRNA-26a in cisplatin-resistant SGC-7901/DDP cells and parent SGC-7901 cells was evaluated by qRT-PCR. The effect of miR-26a on sensitivity of GC cells to cisplatin was assayed using MTS method. The effect of miR-26a on cisplatin-induced apoptosis were determined by Annexin V/propidium iodide (PI) double staining method and flow cytometry. The targets of miR-26a were identified using a luciferase activity assay and miR-26a-mediated target genes expression analysis. Furthermore, the role of the targets neuroblastoma RAS viral (v-ras) oncogene homolog (NRAS) and E2F2 on sensitivity of chemotherapy in GC by MTS and apoptotic cell analysis was assessed. Results: We found that miR-26a was downregulated in cisplatin-resistant SGC-7901/DDP cells compared with SGC-7901 cells. Using both gain- and loss-of-function analyses, we further revealed that miR-26a could improve the sensitivity of GC cells to cisplatin. Furthermore, miR-26a has target sites in the 3′-UTR of NRAS and E2F2 by luciferase reporter assay and reduces the expression levels of NRAS and E2F2. In addition, knockdown of NRAS or E2F2 sensitize GC cells to cisplatin. Conclusion: Our results suggest that miR-26a can improve the sensitivity of GC cells to cisplatin-based chemotherapies through targeting NRAS and E2F2, and provide the first evidence of the potential utility of miR-26a as a sensitizer in chemotherapy for GC.


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