American Association for Cancer Research
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00085472can072238-sup-suppl_fig_1.pdf (411.57 kB)

Supplementary Figure 1 from Nitric Oxide Inactivates the Retinoblastoma Pathway in Chronic Inflammation

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posted on 2023-03-30, 17:48 authored by Lei Ying, Anne B. Hofseth, Darren D. Browning, Mitzi Nagarkatti, Prakash S. Nagarkatti, Lorne J. Hofseth
Supplementary Figure 1 from Nitric Oxide Inactivates the Retinoblastoma Pathway in Chronic Inflammation

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ARTICLE ABSTRACT

Patients with chronic inflammatory bowel disease have a high risk of colon cancer. The molecules that initiate and promote colon cancer and the cancer pathways altered remain undefined. Here, using in vitro models and a mouse model of colitis, we show that nitric oxide (NO) species induce retinoblastoma protein (pRb) hyperphosphorylation and inactivation, resulting in increased proliferation through the pRb-E2F1 pathway. NO-driven pRb hyperphosphorylation occurs through soluble guanylyl cyclase/guanosine 3′,5′-cyclic monophosphate signaling and is dependent on the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase MEK/ERK and phosphatidylinositol 3-kinase/AKT pathways. Our results reveal a link between NO and pRb inactivation and provide insight into molecules that can be targeted in the prevention of the inflammation-to-cancer sequence. [Cancer Res 2007;67(19):9286–93]

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