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Neamine Inhibits Tumor Growth In a Mouse Model of Colitis-Associated Cancer
Alexander Hu1, James Yoo1 1 Brigham and Women's Hospital, Boston, MA

Background: We have previously shown that angiogenin, a 14-kDa ribonuclease, regulates colitis severity and tumor growth in a mouse model of colitis-associated cancer (CAC). The aim of this study was to determine whether pharmacologic inhibition of angiogenin can be used therapeutically in CAC.

Methods: Wild-type (WT) C57BL/6 mice (n=27) were given azoxymethane (AOM), a colon carcinogen, 2 days in advance of two cycles of 3.5% dextran sodium sulfate (DSS). Neamine (30 mg/kg, IP every 3 days), an angiogenin inhibitor, was given starting on day 0 (n=5), after the 1st DSS cycle (n=8), and after the 2nd DSS cycle (n=7). Disease activity index (DAI) was recorded, and mice were euthanized after the 2nd DSS cycle and were compared to control mice (n=7).

Results: The administration of neamine was associated with more severe colitis during the recovery phase of colitis but led to a significant reduction in tumor number (control: 16.9 9.5; neamine: 10.6 5.3, p=0.038). Mice given neamine at baseline (10.0 3.4 tumors), after the 1st DSS cycle (10.63 5.7) and after the 2nd DSS cycle (10.86 6.5) all developed fewer tumors compared to the control group. The effectiveness of neamine to suppress tumor growth diminished when administered late vs. early.

Conclusion: The angiogenin inhibitor neamine worsens colitis but decreases tumor growth in a mouse model of CAC. These findings mirror the phenotypic responses of Ang1-KO mice to AOM-DSS and suggest that targeted inhibition of angiogenin may be a novel therapeutic strategy for CAC.
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