Metformin inhibits β-catenin phosphorylation on Ser-552 through an AMPK/PI3K/Akt pathway in colorectal cancer cells

Several epidemiologic studies have revealed strong inverse associations between metformin use and risk of colorectal cancer development. Nevertheless, the underlying mechanisms are still uncertain. The Wnt/β-catenin pathway, which plays a central role in intestinal homeostasis and sporadic colorectal cancer development, is regulated by phosphorylation cascades that are dependent and independent of Wnt. Here we report that a noncanonical Ser552 phosphorylation in β-catenin, which promotes its nuclear accumulation and transcriptional activity, is blocked by metformin via AMPK-mediated PI3K/Akt signaling inhibition.

Palabras clave: AMPK , COLORECTAL CANCER , METFORMIN , PI3K/AKT , BETA-CATENIN

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Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)

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URI: http://hdl.handle.net/11336/110681

DOI: https://doi.org/10.1016/j.biocel.2019.05.004

URL: https://www.sciencedirect.com/science/article/abs/pii/S1357272519300986

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Articulos(INIGEM)
Articulos de INSTITUTO DE INMUNOLOGIA, GENETICA Y METABOLISMO

Articulos(ININFA)
Articulos de INST.DE INVEST.FARMACOLOGICAS (I)

Citación

Amable, Gastón Federico; Martínez León, Eduardo Antonio; Picco, María Elisa; Di Siervi, Nicolás; Davio, Carlos Alberto; et al.; Metformin inhibits β-catenin phosphorylation on Ser-552 through an AMPK/PI3K/Akt pathway in colorectal cancer cells; Pergamon-Elsevier Science Ltd; International Journal of Biochemistry and Cellular Biology; 112; 10-5-2019; 88-94

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