ArticleProceedings of the National Academy of Sciences of the United States of America1997
Induction of minisatellite mutation in NIH 3T3 cells by treatment with the tumor promoter okadaic acid.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 48 citations in OpenAlex.
- Article
- Article
- Cell Death Inducing Microbial Protein Phosphatase Inhibitors--Mechanisms of Action.Marine drugs · 2015Review
- Okadaic acid: more than a diarrheic toxin.Marine drugs · 2013Review
- A truncated isoform of the protein phosphatase 2A B56gamma regulatory subunit may promote genetic instability and cause tumor progression.The American journal of pathology · 2003Article
- Unfolding of quadruplex structure in the G-rich strand of the minisatellite repeat by the binding protein UP1.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Frequent and multiple mutations at minisatellite loci in sporadic human colorectal and gastric cancers--possible mechanistic differences from microsatellite instability in cancer cells.Japanese journal of cancer research : Gann · 2002Article
- Minisatellite instability in severe combined immunodeficiency mouse cells.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Okadaic acid (OA) is a strong tumor promoter of mouse skin carcinogenesis and also a potent inhibitor of serine/threonine protein phosphatases. OA induces various genetic alterations in cultured cells, such as diphtheria-toxin-resistance mutations, sister chromatid exchange, exclusion of exogenous transforming oncogenes, and gene amplification. The present study revealed that it caused minisatellite mutation (MSM) at a high frequency in NIH 3T3 cells, although no microsatellite mutation was found. Nine of 31 clones (29%) exhibited MSM after 6 days of OA treatment, as opposed to only 1 of 30 clones (3%) without OA exposure. Moreover, NIH 3T3 cells treated with OA acquired tumorigenicity in nude mice, giving rise to 7 tumors within 25 weeks in 20 sites where 3 x 10(6) cells were injected. In contrast, the same numbers of untreated cells gave rise to only one tumor, and the tumor grew much slower. All of three OA-induced tumors examined manifested the MSM. The findings thus point to a molecular mechanism by which OA could function as a tumor promoter, and also the biological relevance of the induction of MSM in the tumorigenic process by OA.
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