|In the present study, we investigated the involvement of Chmp1 (Chromatin Modifying Protein 1/Charged Multivesicular body Protein 1) in the development of mouse pancreatic acinar tumor cell line. CRL 2151 cell line was transfected with Chmp1/CS2 vector to compare growth, morphology and expression of Chmp1, p53 and pp53 (ser 37) with control-transfected cells. CRL 2151 cells were treated with all-trans retinoic acid (ATRA) to compare growth, morphology and expression of Chmp1 and p53 with control-treated cells. Strabismus was used as control. Results showed inhibition of growth but no morphological change in transfected cells. Western blot analysis showed that Chmp1 transfection upregulated the expression of p53, pp53 and Stbm temporarily. Treatment of cells with ATRA did not inhibit growth or show morphological change. However, Western blot analysis demonstrated the upregulation of Chmp1, p53 and Stbm proteins. Microarray analysis of samples transfected with Chmp1 or treated with retinoic acid was done to determine if the same set of genes will be regulated. The pro-apoptotic genes Bad and Bak are among the genes up-regulated. Cell division cycle protein, Cdca7, was among the genes down-regulated. Results from Western blot analysis confirmed the expression of Bad and Bak genes. Taken together, these results suggest that Chmp1 functions in the suppression of pancreatic tumor by the retinoic acid signaling pathway.