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Effects of glabridin combined with 5-fluorouracil on the proliferation and apoptosis of gastric cancer cells

机译:加拉必定联合5-氟尿嘧啶对胃癌细胞增殖和凋亡的影响

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摘要

Gastric cancer most commonly occurs in East Asia, and China accounts for more than half the of world's gastric cancer burden. Despite the efficacy of chemotherapy for patients, this treatment leads to significant patient inconvenience, toxicity and cost. The present study aimed to assess a non-toxic agent, glabridin, as a future chemotherapeutic approach for treating gastric cancer. Using cell proliferation, apoptosis, invasion, and colony formation assays, it was determined that glabridin alone, or in combination with 5-fluorouracil (5-FU), inhibited MKN-45 cell proliferation and invasion, and increased apoptosis. These effects were accompanied by downregulation of p16, E-cadherin and apoptosis regulator Bcl-2 protein, and upregulation of N-cadherin, apoptosis regulator BAX and caspases 3, 8 and 9. The results demonstrated that glabridin may inhibit the malignant proliferation of the human gastric cancer MKN-45 cell line and enhance the efficiency of 5-FU. The data indicate that the p16, and potentially the p16/cyclin-dependent kinase 4/cyclin D1 pathway, may be a novel target for gastric cancer therapy.
机译:胃癌最常见于东亚,而中国占世界胃癌负担的一半以上。尽管化学疗法对患者有效,但是这种治疗导致显着的患者不便,毒性和成本。本研究旨在评估一种无毒药物加拉帕丁,作为未来治疗胃癌的化学疗法。使用细胞增殖,凋亡,侵袭和集落形成测定法,确定了格拉德汀单独或与5-氟尿嘧啶(5-FU)组合抑制MKN-45细胞增殖和侵袭,并增加了凋亡。这些作用伴随着p16,E-钙粘着蛋白和凋亡调节剂Bcl-2蛋白的下调,以及N-钙粘着蛋白,凋亡调节剂BAX和胱天蛋白酶3、8和9的上调。结果表明,麦角蛋白可能抑制了其的恶性增殖。人胃癌MKN-45细胞系可增强5-FU的效率。数据表明,p16,可能还有p16 / cyclin依赖性激酶4 / cyclin D1途径,可能是胃癌治疗的新靶标。

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