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Increased Expression of Human Ribosomal Phosphoprotein P0 Messenger RNA in Hepatocellular Carcinoma and Colon Carcinoma¹

Division of Cellular and Molecular Biology, Dana-Farber Cancer Institute [G. F. B., S. B., M. L., L. B. C.]; Department of Surgery, New England Deaconess Hospital [R. S., K. M., G. D. S.]; and Division of Gastroenterology, Brigham & Women's Hospital [J. L. G., G. F. B.], Harvard Medical School, Boston, MA 02115

To search for differentially expressed gene products in selected cancers of endodermal origin, cDNA libraries derived from mRNA in human hepatocellular carcinoma and adjacent grossly normal tissue were generated. From these parent libraries, subtracted cDNA libraries of tumor minus normal and normal minus tumor tissues were constructed. After screening these subtracted libraries by ± hybridization, a cDNA clone that is overexpressed in hepatocellular carcinoma and encodes the human acidic ribosomal phosphoprotein P0 (P0) was identified. We then evaluated the expression of this phosphoprotein P0 in human colon carcinoma samples. Surgical specimens of primary tumors and liver metastases were examined by Northern hybridization of total RNA with one of 2 ³²P-labeled P0 probes. The mRNA level of the P0 was greater in primary colon carcinoma than in paired adjacent normal colonic epithelium in 36 of 38 cases; the mean tumor/normal ratio was 2.7 (range, up to 13). The tumor/normal ratio, when plotted against the Dukes' stage of disease, gave evidence for increasing P0 expression with increasing stage of colon carcinoma (P = 0.02). In all 8 cases of paired colon carcinoma metastatic to liver and 2 cases of paired primary hepatocellular carcinoma, the P0 mRNA level was greater in tumor than in adjacent normal liver tissue. The mean tumor/normal ratio was 4.0 (range, up to 11) for the colon cancers metastatic to liver and 4.2 for the primary hepatocellular carcinoma samples. These findings support a common increased expression of selected gene products in different tumors of endodermal origin and suggest that increased P0 expression, in line with certain other ribosomal proteins, may be associated with human colorectal cancer progression and biological aggressiveness.

¹ This work was supported by NIH Grants CA44704 and DK07533. G. F. B. is the recipient of National Research Service Award Grant 1F32 CA-0900 from the National Cancer Institute. Presented in part at the annual meeting of the American Gastroenterological Association, New Orleans, LA, 1991 (34).

² Present address: Second Department of Surgery, University of Tokyo 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan.

³ To whom requests for reprints should be addressed, at Division of Cellular and Molecular Biology, Mayer 840, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115.

Received 7/23/91. Accepted 3/24/92.

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