Liraglutide, a glucagon-like peptide-1 analog, induce autophagy and senescence in HepG2 cells
Liraglutide, a glucagon-like peptide-1 analog, induce autophagy and senescence in HepG2 cells
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DOI：
10.1016/j.ejphar.2017.05.015
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发表时间：
2017-08-15
影响因子：
5
通讯作者：
de Oliveira, Jarbas Rodrigues
中科院分区：
文献类型：
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作者：
Krause, Gabriele Catyana;Lima, Kelly Goulart;de Oliveira, Jarbas Rodrigues
据报道，胰高血糖素样肽 1 (GLP-1) 药物与癌症风险增加以及肿瘤生长和转移的抑制有关。本研究的目的是评估利拉鲁肽对肝细胞癌细胞HepG2的作用。细胞计数用于评估与细胞增殖减少相关的机制。还使用核染色和形态分析来验证利拉鲁肽治疗后发生的过程，并且为了更好地理解该机制，进行了 TGF-β1 分析。利拉鲁肽治疗后 HepG2 细胞的增殖减少，但氧化应激水平没有改变。利拉鲁肽能够通过增加 TGF-β1 诱导自噬和衰老，这可能解释了生长下降。我们已经证明，利拉鲁肽在 HepG2 细胞中具有抗增殖作用，通过增加 TGF-β1 诱导自噬和衰老。
It has been reported that glucagon-like peptide-1 (GLP-1) agents have been associated with both the increased risk of cancer and inhibition of tumor growth and metastases. The aim of this study is to evaluate the effect of liraglutide on hepatocellular carcinoma cells - HepG2. Cytometry was used to evaluate mechanism related to decreased cell proliferation. Nuclear staining and morphometric analysis were also used to verify the process that was taking place after treatment with liraglutide, and in order to better understand the mechanism, TGF-beta 1 was performed. HepG2 cells decreased proliferation after liraglutide treatment without altering oxidative stress levels. Liraglutide was able to induce autophagy and senescence through the increase of TGF-beta 1 which possibly explains the growth decrease. We have demonstrated that liraglutide has an antiproliferative effect in HepG2 cells inducing autophagy and senescence by the increase of TGF-beta 1.