Journal Article

Involvement of glutathione in induction of c-<i>jun</i> proto-oncogene by methylmethanesulfonate in NIH 3T3 cells

Min-Liang Kuo, Tzu-Ching Meng and Jen-Kun Lin

in Carcinogenesis

Volume 17, issue 4, pages 815-820
Published in print April 1996 | ISSN: 0143-3334
Published online April 1996 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/17.4.815
Involvement of glutathione in induction of c-jun
                    proto-oncogene by methylmethanesulfonate in NIH 3T3 cells

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The c-jun proto-oncogene plays a vital role in the carcinogenic process. Although numerous words have extensively investigated the induction mechanisms of c-jun by UV, hydrogen peroxide or 12-O-tetradecanoylphorbol-13-acetate, the mechanism induced by alkylating agents has received little attention. In this study, NIH 3T3 cells were exposed to methylmethanesulfonate (MMS), revealing that the agent clearly induced c-jun expression with a peak at 2 h. Pretreatment of cells with various kinase inhibitors, e.g. H7, genistein, herbimycin A and tyrphostin, did not show any significant effects on the MMS-induced c-jun expression. Benzamide, aninhibitor of poly(ADP)-ribosylation, enhanced the MMS-induced DNA breakages, but did not protentiate that agent which elicited c-jun expression. Another experiment showed that this agent transfected and overexpressed an activated v-H-ras gene in NIH 3T3 cells, which became more resistant to MMS-induced DNA damage but expressed thesame level of c-jun transcript as compared with NIH 3T3 cells in response to MMS. If intracellular glutathione (GSH) was completely depleted by buthionine sulfoximine (BSO), the MMS-elicted c-jun expression wasblocked. Subsequently, re-elevating intracellular GSH by washing off BSO caused the expression of c-jun by MMS to increase proportionately. Based on these findings, we can conclude that the mechanism by which MMS induced c-jun expression does not occur through activation of protein tyrosine kinases or initiation of DNA damage, butis closely related to the intracellular GSH.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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