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Liraglutide, a glucagon-like peptide-1 analog, induce autophagy and senescence in HepG2 cells.

Eur J Pharmacol · 2017

Last updated 2026-05-28

In a lab study, the GLP-1 drug liraglutide reduced the growth of liver cancer cells (HepG2) without changing oxidative stress levels. The drug triggered two processes—autophagy (cell cleanup) and senescence (cell aging)—likely by increasing levels of a protein called TGF-β1.

AI summary of the abstract below.

JournalEur J Pharmacol, 2017
Citations35
Relative citation ratio1.35
NIH percentile61
Molecules liraglutide
Conditions studied Mash

Abstract

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-β1 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-β1 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-β1.

Verbatim abstract via PubMed 28501576 ↗

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