ArticleCurrent cancer drug targets2010
Bid mediates anti-apoptotic COX-2 induction through the IKKbeta/NFkappaB pathway due to 5-MCDE exposure.
Article in Current cancer drug targets, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Although Bid has been considered as a cell apoptotic mediator, current studies suggest a possible role in cell survival in mouse embryonic fibroblasts (MEFs) response to low doses of anti-(+/-)-5- methylchrysene-1,2-diol-3,4-epoxide(<or=0.25 microM) (5-MCDE). We found that exposure of MEFs to 0.25 microM 5-MCDE resulted in a slight apoptotic induction, while this apoptotic response was substantially increased in the Bid knockout MEFs (Bid(-/-)), suggesting Bid-mediated anti-apoptotic function in this response. This notion was further supported by the findings that re-constitution expression of Bid into Bid(-/-) cells could inhibit the increased apoptosis. Further studies showed that Bid anti-apoptotic function was associated with its mediation of COX-2 expression, which was based on the results of the reduction of COX-2 expression in Bid(-/-) cells, restoration of low sensitivity to 5-MCDE apoptotic response by the introduction of Bid into Bid(-/-) cells and increased sensitivity of WT MEFs to 5-MCDE apoptosis by knockdown of COX-2 expression. Furthermore, Bid mediated COX-2 expression through the IKKbeta/NFkappaB pathway because the deficiency of Bid in Bid(-/-) MEFs resulted in blockade of IKK/NFkappaB activation and knockout of IKKbeta caused abrogation of COX-2 expression induced by 5-MCDE. Collectively, our results demonstrate that Bid is critical for COX-2 induction through the IKKbeta/NFkappaB pathway, which mediates its anti-apoptotic function, in cell response to low doses of 5-MCDE exposure.
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