INVERSE MODULATION OF STEADY-STATE MESSENGER-RNA LEVELS OF 2 NONINTEGRIN LAMININ-BINDING PROTEINS IN HUMAN COLON-CARCINOMA

CASTRONOVO*, E CAMPO, FA VANDENBRULE, AP CLAYSMITH, CIOCE, FT LIU, PL FERNANDEZ, ME SOBEL

*Corresponding author for this work

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105 Citations (Web of Science)

Abstract

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 downregulated (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

Original languageEnglish
Pages (from-to)1161-1169
Number of pages9
JournalJournal of the National Cancer Institute
Volume84
Issue number15
DOIs
Publication statusPublished - 5 Aug 1992

Keywords

  • TUMOR-CELLS
  • EXTRACELLULAR-MATRIX
  • MOLECULAR-CLONING
  • RECEPTOR
  • EXPRESSION
  • LECTIN
  • METASTASIS
  • CANCER
  • GLYCOPROTEIN
  • PROGRESSION

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