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Arrest in late G 2 or prophase of cell cycle induced by 4,4‐(l,2‐ethanediyl) bis (1‐isobutoxycarbonyloxymethyl 2, 6‐piperazinedione) (MST‐16) in cultured l1210 cells
Author(s) -
Liu YunPeng,
Araya ShinIchi,
Nakamura Toru
Publication year - 1992
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/ijc.2910510521
Subject(s) - cell cycle , etoposide , vincristine , l1210 cells , dna synthesis , cell growth , growth inhibition , biology , cell cycle checkpoint , thymidine , in vitro , flow cytometry , cytotoxicity , cell , cancer research , cell culture , microbiology and biotechnology , chemotherapy , biochemistry , genetics , cyclophosphamide
The effects of MST‐16, a new antitumor agent derived from bis (2, 6‐dioxopiperazine), on cell growth, cell‐cycle progression and DNA synthesis, alone and in combination with other antitumor agents, were investigated in murine leukemia L1210 cells in vitro. The drug showed dose‐dependent inhibition of cell growth, and this effect was cell‐cycle phase‐specific. Flow cytometric analysis indicated that the drug could retard‐arrest the cells in late G 2 phase or prophase and that it did not affect the progression from G 1 to G 2 phase. In the presence of MST‐16, the change in 3 H‐thymidine incorporation was proportional to the retardation‐arrest of the cells, suggesting that MST‐16 has no direct action on DNA synthesis itself. MST‐16 could continuously retard the cells which were arrested by etoposide (VP‐16); and vincristine (VCR) could block the progression of the cells arrested by MST‐16, but not vice versa. The addition of MST‐16 followed by VCR was more effective than simultaneous addition of the 2 drugs on inhibition of cell growth. These results will be useful in designing a reasonable regimen of MST‐16 chemotherapy for malignancies. © 1992 Wifey‐Liss, Inc.