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Departments of Urology [D. I. K., C. P. N. D., J. T. H.], Thoracic Surgery [W-W. Z.], Hematology [N. T. V.], and Molecular Pathology [S-H. L.], The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030
Recently, we demonstrated that an immunoglobulin-like cell adhesion molecule, C-CAM, acts as a tumor suppressor in prostate cancer. It is known that C-CAM is expressed in many epithelial cell types. In this study, we tested the possibility that C-CAM may also suppress bladder cancer progression. We used an orthotopic tumor model, which provides a relevant organ condition for examining the interaction between primary tumor cells and their microenvironment; this interaction has a critical impact on the behavior of carcinoma. We constructed a recombinant adenovirus expressing C-CAM1 (an isoform of C-CAM) and infected the 253J B-V cell line, a tumorigenic human bladder carcinoma subline. In vitro, C-CAM1 protein was detected in C-CAM1 adenovirus-infected cells but not in antisense control virus-infected cells, and the levels of expression showed dose dependency. When these cells were injected orthotopically in nude mice, we found that the increased expression of C-CAM1 in the 253J B-V cells repressed the growth of 253J B-V-induced tumors. Taken together, these data indicate that C-CAM1 is a potent tumor suppressor in human bladder cancer.
1 This work was supported in part by an American Cancer Society grant (D. I. K.), NIH Grants GM 43189 (S-H. L.) and CA 59939 (J-T. H.), and Core Grant CA 16672 (to M. D. Anderson Cancer Center).
2 Present address: Baxter Healthcare Corp., Baxter Technology Park, Route 120 and Wilson Road, Round Lake, IL 60073-0490.
3 To whom requests for reprints should be addressed, at Division of Urology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9110. Phone: (214) 648-3988 (phone); Fax: (214) 648-8786.
Received 5/17/96. Accepted 6/14/96.
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