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• W2140147417 abstract "Fumonisin B 1 (FB 1 ) induces apoptosis and decreases the cellular uptake of 5-methyltetrahydrofolate. Two folate transporters (folate receptor, FR, and Reduced Folate Carrier, hRFC1) are involved in the cell uptake of folate. We aimed to study whether FB 1 modifies the expression of the FR and the hRFC1 and whether its apoptotic effect is influenced by folate. Incubation of HepG2 cells with FB 1 induced apoptosis in concentration and time-dependent manner in complete medium (experimental control medium, ECM), as well as in folate-depleted medium (FDM). FDM increased the toxicity of FB 1 as the cells developed apoptosis within 24 h at 1 μM of FB 1 instead of 100 μM in ECM. Whereas FR protein expression in cells grown in ECM was significantly inhibited after apoptosis event, protein expression of the hRFC1 was rather increased. The hrfc1 transcription was decreased in the treated cells. Under folate-deficient conditions, dramatic changes were observed on both transcriptional and post-transcriptional expression of the two transporters. FDM alone reduced FR protein expression by 12 ± 2% and 43 ± 1% at 48 and 72 h, respectively. The 5-methytetrahydrofolate attenuates apoptosis in a greater extent than the folic acid. However, its effects in preventing decrease of both folate transporters have not been observed. In conclusion, this study shows that the changes in the expression of FR after FB 1 addition are probably a consequence of the FB 1 toxicity. The response to FB 1 by HepG2 cell lines is influenced by folate status and by folate form. 5-Methyltetrahydrofolate appears to be more effective in preventing apoptosis than folic acid." @default.
• W2140147417 created "2016-06-24" @default.
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• W2140147417 date "2007-09-07" @default.
• W2140147417 modified "2023-10-17" @default.
• W2140147417 title "Folate receptor and human reduced folate carrier expression in HepG2 cell line exposed to fumonisin B1 and folate deficiency" @default.
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• W2140147417 doi "https://doi.org/10.1093/carcin/bgm149" @default.
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