- Author:
Joo Deuk KIM
1
;
Jung Lim LEE
;
Jeon Han PARK
;
Jae Myun LEE
;
Yeon Hyang KIM
;
Se Jong KIM
Author Information
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords: Malignant melanoma cell lines; ICAM-1; HLA-DR expression; IFN-gamma; transcriptional regulation
- MeSH: Genes, MHC Class II; HLA-DR Antigens/*metabolism; Human; Intercellular Adhesion Molecule-1/*metabolism; Interferon Type II/*pharmacology; Melanoma/*metabolism/pathology; Support, Non-U.S. Gov't; Transcription, Genetic; Tumor Cells, Cultured
- From:Yonsei Medical Journal 1995;36(1):15-25
- CountryRepublic of Korea
- Language:English
- Abstract: Two human malignant melanoma cell lines, Malme-3M and SK-Mel-28, were analyzed for their ability to induce the expression of intercellular adhesion molecule 1 (ICAM-1) and human leukocyte antigen (HLA)-DR molecules on their cell surfaces as well as at the transcriptional level before and after treatment with interferon (IFN)-gamma. Both cell lines demonstrated a high percentage(> 99%) of ICAM-1 expression regardless of IFN-gamma treatment. Before IFN-gamma treatment, Malme-3M cells barely expressed HLA-DR molecules (< 2%) and SK-Mel-28 cells demonstrated a relatively high percentage(> 50%) of HLA-DR expression. Both cell lines displayed elevated levels of HLA-DR expression in a time dependent manner after IFN-gamma treatment. However, these two cell lines have been shown to respond differentially to IFN-gamma. The molecular mechanism underlying such a differential behavior was investigated, and HLA-DR gene regulation was studied at the transcriptional level. Treatment with IFN-gamma led to the steady-state mRNA augmentation of the HLR-DR gene. The HLA-DRA mRNA augmentation was similar in both cell lines, whereas in Malme-3M, IFN-gamma did not augment the rate of transcription of the HLA-DRB gene as much as in SK-Mel-28. Data from this study established the fact that the melanoma cell lines displayed a differential susceptibility to IFN-gamma on the modulation of HLA-DR molecules, and this modulation was transcriptionally regulated.