© 1992 by Oxford University Press
Journal of the National Cancer Institute, Vol. 84, No. 15, 1161-1169,
August 5, 1992
© 1992 Oxford University Press
Inverse Modulation of Steady-State Messenger RNA Levels of Two Non-Integrin Laminin-Binding Proteins in Human Colon Carcinoma
Guest Researcher from the Hospital Clinico Provincial, University of Barcelona, and was a grantee of the Scientific Committee of the North Atlantic Treaty Organization.
Laboratory of Pathology, Division of Cancer Biology, Diagnosis, and Centers, National Cancer Institute Bethesda, Md.
Scripps Clinic and Research Foundation La Jolla, Calif
*Correspondence to: Vincent Castronovo, M.D., Ph.D., National Institutes of Health, Bldg. 10, Rm. 2A33, Bethesda, MD 20892.
Background: Interactions between cells and the basement membrane glycoprotein laminin are altered during colon cancer progression. Colon carcinoma and normal mucosa cells express a variety of laminin-binding proteins, including the 67-kd laminin receptor (67 LR) and a 31-kd human laminin-binding protein (HLBP31) homologous to the 31-kd human IgE-binding protein/galactoside-binding lectin. Purpose: To investigate whether various laminin-binding proteins are differentially expressed in human colon carcinoma, we studied messenger RNA (mRNA) levels of the 67 LR and HLBP31 in matched tumor and adjacent normal mucosa samples from a series of 21 patients. Methods: Total cellular RNA from tumor and normal mucosa was isolated and analyzed by Northern and slot blot hybridization. In addition, HLBP31 protein levels were assessed by the immunoblot technique. Quantitative laminin affinity chromatography was also used to measure the synthesis of HLBP31 protein in five human cancer cell lines. Results: The steady-state mRNA level of HLBP31 was downregu-lated (i.e., decreased) in 18 of 21 human colon carcinomas compared with the level in their corresponding normal colonic mucosa. On average, the level of HLBP31 mRNA was decreased 50% ± 30% (±SD) in the colon cancers. The mean ratio of colon cancer HLBP31 mRNA to adjacent normal mucosa HLBP31 mRNA was twofold lower in primary tumors of patients with metastases (0.3 ± 0.2 SD) than in primary tumors of patients free of metastatic lesions (0.6 ± 0.2 SD). The differences between the two groups of patients were statistically significant (P<.05, Wilcoxon-Mann-Whitney test). We have previously shown that the ratio of colon cancer 67 LR mRNA to corresponding normal mucosa 67 LR mRNA was increased in the same patient population. When the two ratios (ratio of cancer to normal HLBP31 mRNA and ratio of cancer to normal 67 LR mRNA) were compared, HLBP31 mRNA/67 LR mRNA was significantly lower (p<.O5) in primary tumors with metastases (mean ± SD, 0.3 ± 0.2) than in primary cancers without metastases (mean ± SD, 0.7 ± 0.5). The
steady-state level of HLBP31 mRNA was directly correlated with the amount of HLBP31 protein in both colon tissue samples and human cancer cell lines. Conclusion: HLBP31 mRNA expression in colon cancer tissues is modulated inversely to that of 67 LR mRNA expression. The down-regulation of HLBP31 appears to be associated with the metastatic capabilities of colon cancer cells. Implications: Prospective studies on a large cohort should determine if the systematic detection of HLBP31 and 67 LR protein and/ or mRNA can be a valuable adjunct ins the prognostic evaluation of primary colon cancers. [J Natl Cancer Inst 84: 1161–1169, 1992]
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