Effect and Catabolism of All-trans Retinoic Acid in Head and Neck Squamous Cell Carcinoma.
- Author:
Seung Joo YOO
1
;
Hyun Ja KWON
;
Soon Yuhl NAM
;
Sang Yoon KIM
Author Information
1. Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. sykim2@www.amc.seoul.kr
- Publication Type:Original Article
- Keywords:
All-trans retinoic acid;
CYP26;
Cellular retinoic acid binding protein
- MeSH:
Absorption;
Carcinoma, Squamous Cell*;
Cell Line;
Cytochromes;
Head*;
Metabolism*;
Neck*;
Receptors, Retinoic Acid;
Retinol-Binding Proteins, Cellular;
Tretinoin*;
Vitamin A
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
1999;42(12):1541-1546
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: All-trans retinoic acid (RA) is a form of vitamin A analogue that has shown chemopreventive activities in many types of malignancy with the properties that regulate cellular differentiations and suppress malignant proliferations. It is thought that the catabolism of RA is mediated by cytochrome P450RAI (CYP26) and its absorption, effects and catabolism are related to cellular retinol binding proteins (CRBP-I and II) and cellular retinoic acid binding proteins (CRABP-I and II). With eight different squamous cell carcinoma cell lines (AMC-HN-1~-8), we investigated the effects of RA and roles of these proteins in the metabolism and regulatory activity of RA. MATERIALS AND METHODS: Survival fractions of eight AMC-HN cells were analyzed six days after the treating them with 1 nM of RA. Reverse transcription-polymerase chain reactions (RT-PCR) were performed before and 24 hours after the load of 1 nM of RA to detect the expressions of CRBP-I, CRABP-I, CRABP-II, and CYP26. RESULTS: Resistances to RA were detected in AMC-HN-1, -2, -5, and -6 cell lines after RA treatment, and AMC-HN-3, -4, -7, and -8 cell lines showed sensitive responses to RA. Before the addition of RA, expressions of CYP26 were detected in AMC-HN-1, -2, -4, -5, -6, and -7 cell lines and CRBP-I was expressed in AMC-HN-3, 4, 5, 7, and -8. After RA addition, the expressions of CYP26 were enhanced in AMC-HN-2, -5, -6, and -7. In six of eight cell lines, CRABP-I was suppressed and CRABP-II was enhanced after RA treatment. CONCLUSION: These results suggest that CYP26 has a direct correlation with the cellular metabolism of RA in the head and neck squamous cell carcinomas and that CRABP-I and CRABP-II have distinct roles in the regulatory effects of RA. CRBP-I might be an indicator that implies the responsiveness to RA.
