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- W2090032248 abstract "Loss of p16INK4a protein expression has frequently been related to DNA methylation in association with gene silencing. Although the methylation status of exon1α for p16INK4a involvement in various cancers has been extensively analyzed, it has been pointed out that some inconsistencies existed in its relationship to gene silencing of p16INK4a. In this study, we focused on the expression and methylation status in the regions of nt −478 to −201, containing a putative TATA box (nt −401 to −396), and nt −233 to 26, both in a recently cloned 5′ upstream region of rat p16INK4a. We showed that rat lung adenocarcinoma RLCNR did not express the p16INK4a gene, whereas rat osteosarcoma COS1NR and malignant fibrous histiocytoma MFH1NR both expressed it at levels similar to normal fibroblasts, even though the region of nt −233 to 26 was hypermethylated in COS1NR rather than RLCNR. In contrast, the CpG islands near the putative TATA box region were consistently methylated in RLCNR, but not in COS1NR and MFH1NR, as well as in normal fibroblasts. Treatment with 5-aza 2′-deoxycytidine induced expression of p16INK4a gene in RLCNR after 48 h, but no changes were observed in COS1NR and MFH1NR. The results indicated that methylation of CpG islands near a TATA box region played a critical role for gene silencing of the rat p16INK4a gene, rather than that of other regions. © 2003 Wiley-Liss, Inc." @default.
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- W2090032248 date "2003-01-01" @default.
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- W2090032248 title "Expression of thep16INK4a gene and methylation pattern of CpG sites in the promoter region in rat tumor cell lines" @default.
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- W2090032248 doi "https://doi.org/10.1002/mc.10165" @default.
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