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首页> 外文期刊>Journal of Clinical Medicine >Medroxyprogesterone Reverses Tolerable Dose Metformin-Induced Inhibition of Invasion via Matrix Metallopeptidase-9 and Transforming Growth Factor-β1 in KLE Endometrial Cancer Cells
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Medroxyprogesterone Reverses Tolerable Dose Metformin-Induced Inhibition of Invasion via Matrix Metallopeptidase-9 and Transforming Growth Factor-β1 in KLE Endometrial Cancer Cells

机译：Medroxyprogestone逆转可容忍的剂量二甲双胍诱导的侵袭血液侵袭抑制，通过基质金属肽酶-9和转化在KLE子宫内膜癌细胞中的生长因子-β1

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This study was performed to evaluate the anticancer effects of tolerable doses of metformin with or without medroxyprogesterone (MPA) in endometrial cancer cells. Cell viability, cell invasion, and levels of matrix metallopeptidase (MMP) and transforming growth factor (TGF)-β1 were analyzed using three human endometrial adenocarcinoma cell lines (Ishikawa, KLE, and uterine serous papillary cancer (USPC)) after treatment with different dose combinations of MPA and metformin. Combining metformin (0, 100, 1000 μM) and 10 μM MPA induced significantly decreased cell viability in a time- and dose-dependent manner in Ishikawa cells, but not in KLE and USPC cells. In KLE cells, metformin treatment alone significantly inhibited cell invasion in a dose-dependent manner. The inhibitory effect of metformin was reversed when 10 μM MPA was combined, which was significantly inhibited again after treatment of MMP-2/9 inhibitor and/or TGF-β inhibitor. Changes of MMP-9 and TGF-β1 according to combinations of MPA and metformin were similar to those of invasion in KLE cells. In conclusion, the anticancer effects of tolerable doses of metformin varied according to cell type and combinations with MPA. Anti-invasive effect of metformin in KLE cells was completely reversed by the addition of MPA; this might be associated with MMP-9 and TGF-β1.
机译：进行该研究以评估耐受剂量二甲双胍的抗癌效果，其中子宫内膜癌细胞中的细胞膜细胞（MPa）。用不同的人子宫内膜腺癌细胞系（Ishikawa，Kle和子宫乳头乳头状乳腺癌（USPC）分析了基质金属肽酶（MMP）和转化生长因子（TGF）-β1的细胞活力，细胞浸润性和转化生长因子（TGF）-β1分析MPA和二甲双胍的剂量组合。组合二甲双胍（0,100,1000μm）和10μMMPa在Ishikawa细胞中以时间和剂量依赖性方式诱导细胞活力显着降低，但不在KLE和USPC细胞中。在Kle细胞中，单独的二甲双胍治疗以剂量依赖性方式显着抑制细胞侵袭。当合并10μMMPa时，二甲双胍的抑制作用反转，在治疗MMP-2/9抑制剂和/或TGF-β抑制剂后再次显着抑制。根据MPa和二甲双胍组合的MMP-9和TGF-β1的变化与KLE细胞中的侵袭相似。总之，耐受剂量二甲双胍的抗癌效应根据细胞类型和MPa组合而变化。通过添加MPa完全反转kle细胞中二甲双胍的抗侵入作用;这可能与MMP-9和TGF-β1相关联。

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