Abstract
The High Mobility Group A1 (HMGA1) proteins are a class of oncogenes whose specific role in colon and other cancers is currently emerging. Our analysis of the HMGA1 promoter region revealed several putative sites for beta‐catenin/tcf binding suggesting that HMGA1 may be activated by the adenomatous polyposis coli (Apc)/beta‐catenin pathway in colon cancer. To better understand the specific role of HMGA1 in colon carcinoma formation, we evaluated the expression of HMGA1 in the Apc/min colon cancer mouse model. Results of quantitative real‐time RT‐PCR (qRT‐PCR) show a 9‐fold increase over normal intestine in HMGA1 mRNA where Apc is truncated and in tumors. Consistent with qRT‐PCR data, HMGA1 protein levels were also significantly higher in Apc‐min intestinal tumors than those from normal mouse tissues. To determine if Apc/beta catenin signaling directly impacts HMGA1 expression, we tested the effect of Apc recovery on HMGA1 expression. Preliminary results indicate that zinc‐induced full‐length Apc expression suppresses HMGA1 levels and that truncations in Apc may activate HMGA1 to promote cancer initiation and progression. Collectively, these results provide the first line of evidence supporting the cooperation of truncated Apc and HMGA1 in colon cancer.This project was supported by NIH grant P20 RR‐16461 in support of SC INBRE.
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