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Mismatch repair and microsatellite instability in esophageal cancer cells
Author(s) -
Uchida Nobuhiro,
Kumimoto Hiroshi,
Nishizawa Kimiko,
Tokumasu Sachiko,
Harada Hideki,
Shimada Yutaka,
Ishizaki Kanji
Publication year - 2001
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/1097-0215(200002)9999:9999<::aid-ijc1106>3.0.co;2-m
Subject(s) - dna mismatch repair , microsatellite instability , genome instability , esophageal cancer , biology , cancer research , dna repair , microbiology and biotechnology , microsatellite , dna , cell culture , in vitro , cancer , gene , dna damage , genetics , allele
Using in vitro mismatch repair (MMR) assay, we have identified 3 of 22 esophageal cancer cell lines exhibiting reduced MMR activity. By means of gel‐shift assay, decreased binding ability to GT mismatch and CA loop was observed in these 3 cell lines. However, we could not find any mutations in the hMSH2, hMSH3 and hMSH6 genes, the protein products of which exhibit mismatch binding activity in human cells. In addition, when using antibodies against 5 MMR‐related proteins (hMSH2, hMSH3, hMSH6, hPMS2 and hMLH1), no aberrant expression was detected in any of them. When we examined 9 microsatellite loci in endogenous genomic DNA, these 3 esophageal cancer cell lines, deficient in MMR, did not exhibit microsatellite instability. However, when we examined the repetitious sequence on exogenous plasmid DNA which was introduced into these 3 esophageal cancer cells, the results suggested that MMR deficiency in esophageal cancer cells could result in moderate instability of the exogenous sequence. © 2001 Wiley‐Liss, Inc.