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Flores, Marcelo B.S; Rocha, Guilherme Z; Damas–Souza, Danilo M; Osório–Costa, Felipe; Dias, Marília M; Ropelle, Eduardo R; Camargo, Juliana A; de Carvalho, Rita B; Carvalho, Hernandes F; Saad, Mario J.A; Carvalheira, José B.C
Gastroenterology (New York, N.Y. 1943), 2012, Volume: 143, Issue: 3Journal Article
Background & Aims Epidemiology studies have shown that obesity increases risk for colorectal cancer (CRC). We investigated the contribution of obesity-induced increases in levels of tumor necrosis factor (TNF)-α and hyperinsulinemia to the development of CRC in mice. Methods Lean and obese mice (C57BL6/J and ob/ob ) were given a combination of azoxymethane and dextran sulfate sodium, which led to the development of CRC; lean and obese severe combined immunodeficient mice were injected with HT-29 cells. We analyzed the roles of TNF-α and insulin in the development of obesity-mediated CRC using immunoblot, immunohistochemical, and apoptosis assays. Results Genetic- and diet-induced obesity increased the incidence and size of tumors that developed after administration of azoxymethane and dextran sulfate sodium, compared with lean mice. HT-29 xenograft tumors grew more rapidly in obese than lean mice. Neutralization of TNF-α reduced activation of c-Jun N-terminal kinase, IκB kinase, and the phosphatidylinositol 3-kinase–Akt–mammalian target of rapamycin signaling pathway; it also reduced the growth and development of tumors in obese mice. Reducing levels of insulin levels had no effect on tumor growth in obese mice. Conclusions TNF-α contributes to colon tumor growth in obese mice. Reagents that inhibit TNF-α might prevent the development or progression of CRC in obese individuals.
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