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Comparative Study
. 2000 Sep;17(3):479-86.

Increased ICAM-1 expression in transformed human oral epithelial cells: molecular mechanism and functional role in peripheral blood mononuclear cell adhesion and lymphokine-activated-killer cell cytotoxicity

G T Huang  1 , X Zhang, N H Park
Affiliations
Comparative Study

Increased ICAM-1 expression in transformed human oral epithelial cells: molecular mechanism and functional role in peripheral blood mononuclear cell adhesion and lymphokine-activated-killer cell cytotoxicity

G T Huang et al. Int J Oncol. 2000 Sep.

Abstract

The intercellular adhesion molecule-1 (ICAM-1, CD54) serves as a counter-receptor for the beta2-integrins, LFA-1 and Mac-1, which are expressed on leukocytes. Although expression of ICAM-1 on tumor cells has a role in tumor progression and development, information on ICAM-1 expression and its role in oral cancer has not been established. Normal human oral keratinocytes (NHOK), human papilloma virus (HPV)-immortalized human oral keratinocyte lines (HOK-16B, HOK-18A, and HOK-18C), and six human oral neoplastic cell lines (HOK-16B-BaP-T1, SCC-4, SCC-9, HEp-2, Tu-177 and 1483) were used to study ICAM-1 expression and its functional role in vitro. Our results demonstrated that NHOK express negligible levels of ICAM-1, whereas immortalized human oral keratinocytes and cancer cells express significantly higher levels of ICAM-1, except for HOK-16B-BaP-T1 and HEp-2. Altered mRNA half-lives did not fully account for the increased accumulation of ICAM-1 mRNA. Adhesion of peripheral blood mononuclear cells (PBMC) to epithelial cells correlated with cell surface ICAM-1 expression levels. This adhesion was inhibited by antibodies specific for either ICAM-1 or LFA-1/Mac-1, suggesting a role for these molecules in adhesion. In contrast, lymphokine-activated-killer (LAK) cell cytotoxic killing of epithelial cells did not correlate with ICAM-1 levels or with adhesion. Nonetheless, within each cell line, blocking of ICAM-1 or LFA-1/Mac-1 reduced LAK cell killing, suggesting that ICAM-1 is involved in mediating this killing.

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Figures

Fig. 1
Fig. 1
Expression of ICAM-1 by primary oral epithelial cells (NHOK) and two immortalized oral epithelial cell lines (HOK-16B and HOK-16B-BaP-T1) containing the HPV-16 genome. (A) Flow cytometric analysis of ICAM-1 expression on oral epithelial cells. Shaded areas represent constitutive ICAM-1 expression and non-shaded areas depict staining with an isotype control antibody. (B) Northern blot analysis of ICAM-1 mRNA expression in oral epithelial cells. Three major ICAM-1 mRNA forms were detected (3.4, 2.6 and 1.7 kb). (C) Relative signal densities of ICAM-1 mRNA among the cells measured by NIH imaging software. Data are from a representative experiment.
Fig. 2
Fig. 2
Expression of ICAM-1 by primary oral epithelial cells (NHOK) and six oral epithelial cell lines (HOK-18A, 1483, HEp-2, SCC-4, SCC-9, and Tu-177). Flow cytometric analysis of ICAM-1 expression on (A) NHOK and three oral cell lines containing HPV-18 and (B) three HPV-negative oral cancer cell lines. Shaded areas represent constitutive ICAM-1 expression and non-shaded areas depict staining with an isotype control antibody. (C) Northern blot analysis of ICAM-1 mRNA expression in oral epithelial cells. (D) Relative signal densities of ICAM-1 mRNA among the cells measured by NIH imaging software. Data are from a representative experiment.
Fig. 3
Fig. 3
Relative cell surface ICAM-1 expression on NHOK and oral epithelial cell lines. Δ mean fluorescence intensity (MFI) = MFI with anti-ICAM-1 IgG minus MFI with isotype control. Data represent mean ± SEM of the results of at least two or more independent experiments.
Fig. 4
Fig. 4
ICAM-1 mRNA half-lives in oral epithelial cells. At different time points (0, 0.5, 1, 2, 4 and 6 h) following ActD treatment, RNA were isolated and subjected to Northern blot analysis. Northern blot images and plots to determine the message half-lives are shown. The signal densities of ICAM-1 mRNA were measured by NIH imaging software. T1/2, mRNA half-life.
Fig. 5
Fig. 5
Relative levels of PBMC adherence to NHOK and oral epithelial cell lines. The amount of bound PBMC was measured as the percentage of the total PBMC added to the monolayers before removal of the unbound PBMC. Data are presented as mean ± SEM of the results of at least two or more independent experiments.
Fig 6
Fig 6
Relative levels of LAK cell cytotoxicity to oral epithelial cells. Data are presented as mean ± SEM of the results of at least two or more independent experiments except where indicated. N.D., not determined. *, single experiment.
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