Curcumin Promoted miR-34a Expression and Suppressed Proliferation of Gastric Cancer Cells

姜黄素 细胞周期 细胞周期蛋白D1 细胞生长 细胞凋亡 癌症研究 分子生物学 流式细胞术 化学 癌细胞 生物 癌症 药理学 生物化学 遗传学
作者
Chunlin Sun,Shuping Zhang,Changhai Liu,Xueqiang Liu
出处
期刊:Cancer Biotherapy and Radiopharmaceuticals [Mary Ann Liebert, Inc.]
卷期号:34 (10): 634-641 被引量:73
标识
DOI:10.1089/cbr.2019.2874
摘要

Background: To investigate the effects of curcumin on miR-34a and proliferation of gastric cancer cells. Materials and Methods: Human gastric cancer cell line SGC-7901 was divided into control, curcumin, miR-34a agomir (miR-34a), miR-34a agomir negative control, and curcumin combined miR-34a antagomir (combine) groups. 3-(4, 5-dimethylthiazolyl-2)-2, 5-diphenyltetrazolium bromide assay, scratch damage test, and transwell assay were used to detect cell proliferation, migration, and invasion. The cell apoptosis and cell cycle were detected by flow cytometry. Western blot was used to detect the expression of B-cell lymphoma-2 (Bcl-2), cyclin-dependent kinase 4 (CDK4), and cyclin D1. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling was used to detect apoptosis of tumors and Western blot was used to detect the expression of Bcl-2, CDK4, and cyclin D1 in tumors. Results: The results showed that curcumin markedly increased the content of miR-34a microRNA (mRNA) in SGC-7901 cells, inhibited proliferation, migration, and invasion of SGC-7901 cells, when compared to control group (p < 0.05). Compared with control group, curcumin significantly inhibited cell cycle progression in G0/G1-S phase, increased the cell number of G0/G1 phase, and downregulated the Bcl-2, CDK4, and cyclin D1 protein expression in cells and tissues (p < 0.05). After transfection of miR-34a agomir or antagomir into cells it was found that miR-34a agomir and curcumin had similar effects on resisting malignant biological behavior. Curcumin combined with miR-34a antagomir could weaken or reverse the above results. Conclusions: Curcumin could inhibit the proliferation and induce apoptosis of SGC-7901 cells. Its mechanism might be related to the miR-34a expression in cells, thus affecting the expression of Bcl-2, CDK4, and cyclin D1.
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