Quercetin Reverses Rat Liver Preneoplastic Lesions Induced by Chemical Carcinogenesis

Author:

Carrasco-Torres Gabriela1ORCID,Monroy-Ramírez Hugo Christian2,Martínez-Guerra Arturo Axayacatl1,Baltiérrez-Hoyos Rafael3,Romero-Tlalolini María de los Ángeles3,Villa-Treviño Saúl1,Sánchez-Chino Xariss4,Vásquez-Garzón Verónica Rocío13ORCID

Affiliation:

1. Departamento de Biología Celular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México, Mexico

2. Departamento de Farmacología, Facultad de Medicina Mexicali, Universidad Autónoma de Baja California, Baja California, Mixicali, BC, Mexico

3. CONACYT, Facultad de Medicina y Cirugía, Universidad Autónoma Benito Juárez de Oaxaca, Oaxaca de Juárez, OAX, Mexico

4. Dirección de Investigación y Desarrollo Tecnológico, Universidad Politécnica Mesoamericana, Tenosique, TAB, Mexico

Abstract

Quercetin is a flavonoid widely studied as a chemopreventive agent in different types of cancer. Previously, we reported that quercetin has a chemopreventive effect on the liver-induced preneoplastic lesions in rats. Here, we evaluated if quercetin was able not only to prevent but also to reverse rat liver preneoplastic lesions. We used the modified resistant hepatocyte model (MRHM) to evaluate this possibility. Treatment with quercetin was used 15 days after the induction of preneoplastic lesions. We found that quercetin reverses the number of preneoplastic lesions and their areas. Our results showed that quercetin downregulates the expression of EGFR and modulates this signaling pathway in spite of the activated status of EGFR as detected by the upregulation of this receptor, with respect to that observed in control rats. Besides, quercetin affects the phosphorylation status of Src-1, STAT5, and Sp-1. The better status of the liver after the treatment with quercetin could also be confirmed by the recovery in the expression of IGF-1. In conclusion, we suggest that quercetin reversed preneoplastic lesions by EGFR modulation and the activation state of Src, STAT5, and Sp1, so as the basal IGF-1.

Funder

Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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