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- Bochao Zhao, Jiale Zhang, Xiuxiu Chen, Huimian Xu, and Baojun Huang.
- Department of Surgical Oncology, First Affiliated Hospital, China Medical University, Shenyang, China.
- Arch Med Sci. 2019 Mar 1; 15 (2): 498-503.
IntroductionGastric cancer is one of the most common cancers of the digestive system and is associated with high morbidity and mortality. The aim of this study was to investigate whether miR-26b is involved in the proliferation and resistance to paclitaxel chemotherapy in gastric cancer cells.Material And MethodsThe expression of miR-26b in gastric cancer cell lines was determined by quantitative real-time PCR. Bioinformatics software was used to predict potential target genes of miR-26b. Luciferase assay was used to verify the interactions between target genes and miR-26b. CDC6 protein expression was measured by Western blot. The proliferation and chemotherapy resistance were analyzed by MTT assay. Cell invasion was evaluated by Transwell assay.ResultsMiR-26b was down-regulated in gastric cancer cell lines compared to normal control cells, and its expression in drug resistance cells was even lower (p < 0.05). CDC6 was identified as a potential target gene of miR-26b by using bioinformatics analysis software. The expression of CDC6 was inhibited by miR-26b both at RNA level, which was determined by luciferase assay, and at protein level, which was determined by Western blot (p < 0.05). Silencing CDC6 inhibited cell proliferation, invasion, and promoted apoptosis of gastric cancer cell lines, BGC823 and SGC7901 (p < 0.05). Moreover, CDC6 knockdown inhibited chemotherapy resistance to paclitaxel, IC50 to paclitaxel decreased from 153.17 ±0.49 μg/l to 39.81 ±0.28 μg/l (p < 0.05).ConclusionsmiR-26b inhibits growth and resistance to paclitaxel chemotherapy by silencing the CDC6 gene in the gastric cancer cell line SGC7901.
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