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Conditional expression of MCM7 increases tumor growth without altering DNA replication activity
Author(s) -
Yoshida Kenichi,
Inoue Ituro
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)01018-4
Subject(s) - minichromosome maintenance , origin recognition complex , dna replication , eukaryotic dna replication , control of chromosome duplication , biology , helicase , replication factor c , dna replication factor cdt1 , origin of replication , pre replication complex , microbiology and biotechnology , dna , genetics , gene , rna
The minichromosome maintenance (MCM) 2–7 complex is a putative DNA helicase complex that facilitates the initiation of DNA replication. Here, we generated a cell line MCM7 +/− /MCM7‐FLAG, in which one allele of MCM7 is mutated whereas a tetracycline‐repressible promoter could manipulate the expression of exogenous MCM7 protein. Overexpressed MCM7 protein supports efficient DNA replication of Epstein–Barr virus oriP and rapid formation of tumors in nude mice without altering the activity of cellular DNA replication. This system provides a unique setting for studying the function of MCM7 and for screening for potential therapeutics for malignant tumors.