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Exendin-4 does not modify growth or apoptosis of human colon cancer cells.

Endocr Res · 2017

Last updated 2026-05-28

A study tested whether exendin-4, a GLP-1 receptor agonist, affects the growth or survival of human colon cancer cells. The research found no evidence that exendin-4 increased cancer cell proliferation, migration, or resistance to chemotherapy drugs like 5-fluorouracil or irinotecan, nor did it promote tumor growth in animal models.

AI summary of the abstract below.

JournalEndocr Res, 2017
Citations17
Relative citation ratio0.65
NIH percentile36
Molecules

Abstract

AIM: Glucagon-like peptide-1 (GLP-1) receptor agonists are a kind of very popular antidiabetes drugs. They promote cell proliferation and survival through activation of signaling pathways in human islet cells involving phosphate idylinositol 3 kinase (PI3K) and extracellular regulated kinases 1 and 2 (ERK1/2), which are frequently activated in human colon cancer cells. Then, it is possible that taking GLP-1 receptor (GLP-1R) agonists persistently would induce proliferation of β cells as well as colon cancer cells. So, clarifying the effects and mechanisms of GLP-1R agonists on colon cancer cells has important clinical implications. MATERIALS AND METHODS: We investigated GLP-1R expression in human colon cancer tissue samples with immunohistochemisty analysis and explored the effects of exendin-4, a GLP-1 receptor agonist, on colon cancer cells in vitro and in vivo. RESULTS: The results showed lack of GLP-1R expression in both human colon cancer tissues and colon cancer cell lines. Exendin-4 did not enhance the proliferation and migration of colon cancer cell lines in vitro, and nor did it inhibit apoptosis induced by cytotoxic agents such as 5-fluorouracil (5-FU) or irinotecan. In addition, exendin-4 did not promote the propagation of colon cancer cells in vivo. CONCLUSION: Our study suggests that GLP-1R agonists do not modify the growth or survival of human colon cancer cells and may be safe for diabetic patients with colon cancer.

Verbatim abstract via PubMed 28318339 ↗