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培养基更新阻断二甲双胍对培养的MDA-MB-231乳腺癌细胞的抗增殖作用。

Medium Renewal Blocks Anti-Proliferative Effects of Metformin in Cultured MDA-MB-231 Breast Cancer Cells.

作者信息

Rajh Maruša, Dolinar Klemen, Miš Katarina, Pavlin Mojca, Pirkmajer Sergej

机构信息

Faculty of Electrical Engineering, University of Ljubljana, Ljubljana, Slovenia.

Institute of Pathophysiology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia.

出版信息

PLoS One. 2016 May 2;11(5):e0154747. doi: 10.1371/journal.pone.0154747. eCollection 2016.

Abstract

Epidemiological studies indicate that metformin, a widely used type 2 diabetes drug, might reduce breast cancer risk and mortality in patients with type 2 diabetes. Metformin might protect against breast cancer indirectly by ameliorating systemic glucose homeostasis. Alternatively, it might target breast cancer cells directly. However, experiments using MDA-MB-231 cells, a standard in vitro breast cancer model, produced inconsistent results regarding effectiveness of metformin as a direct anti-cancer agent. Metformin treatments in cultured MDA-MB-231 cells are usually performed for 48-96 hours, but protocols describing renewal of cell culture medium during these prolonged treatments are rarely reported. We determined whether medium renewal protocol might alter sensitivity of MDA-MB-231 cells treated with metformin. Using the MTS assay, BrdU incorporation and Hoechst staining we found that treatment with metformin for 48-72 hours failed to suppress viability and proliferation of MDA-MB-231 cells if low-glucose (1 g/L) medium was renewed every 24 hours. Conversely, metformin suppressed their viability and proliferation if medium was not renewed. Without renewal glucose concentration in the medium was reduced to 0.1 g/L in 72 hours, which likely explains increased sensitivity to metformin under these conditions. We also examined whether 2-deoxy-D-glucose (2-DG) reduces resistance to metformin. In the presence of 2-DG metformin reduced viability and proliferation of MDA-MB-231 cells with or without medium renewal, thus demonstrating that 2-DG reduces their resistance to metformin. In sum, we show that medium renewal blocks anti-proliferative effects of metformin during prolonged treatments in low-glucose medium. Differences in medium renewal protocols during prolonged treatments might therefore lead to apparently inconsistent results as regards effectiveness of metformin as a direct anti-cancer agent. Finally, our results indicate that co-therapy with 2-DG and metformin might provide an effective strategy to overcome metformin resistance of breast cancer cells.

摘要

流行病学研究表明,二甲双胍作为一种广泛使用的2型糖尿病药物,可能会降低2型糖尿病患者患乳腺癌的风险及死亡率。二甲双胍可能通过改善全身葡萄糖稳态间接预防乳腺癌。或者,它也可能直接作用于乳腺癌细胞。然而,使用MDA-MB-231细胞(一种标准的体外乳腺癌模型)进行的实验,在二甲双胍作为直接抗癌药物的有效性方面产生了不一致的结果。在培养的MDA-MB-231细胞中进行二甲双胍处理通常持续48 - 96小时,但很少有报告描述在这些长时间处理过程中细胞培养基的更换方案。我们确定培养基更换方案是否会改变用二甲双胍处理的MDA-MB-231细胞的敏感性。通过MTS检测、BrdU掺入和Hoechst染色,我们发现,如果每24小时更换低葡萄糖(1 g/L)培养基,用二甲双胍处理48 - 72小时未能抑制MDA-MB-231细胞的活力和增殖。相反,如果不更换培养基,二甲双胍会抑制它们的活力和增殖。不更换培养基时,培养基中的葡萄糖浓度在72小时内降至0.1 g/L,这可能解释了在这些条件下对二甲双胍敏感性增加的原因。我们还研究了2-脱氧-D-葡萄糖(2-DG)是否能降低对二甲双胍的耐药性。在有2-DG存在的情况下,无论是否更换培养基,二甲双胍都能降低MDA-MB-231细胞的活力和增殖,从而表明2-DG降低了它们对二甲双胍的耐药性。总之,我们表明在低葡萄糖培养基中长时间处理期间,培养基更换会阻断二甲双胍的抗增殖作用。因此,长时间处理过程中培养基更换方案的差异可能导致在二甲双胍作为直接抗癌药物的有效性方面出现明显不一致的结果。最后,我们的结果表明,2-DG与二甲双胍联合治疗可能提供一种克服乳腺癌细胞对二甲双胍耐药性的有效策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e97/4852933/df367a039b31/pone.0154747.g001.jpg

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