ArticleExperimental cell research2013
RAF and antioxidants prevent cell death induction after growth factor abrogation through regulation of Bcl-2 proteins.
Article in Experimental cell research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
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- Metabolism of Reactive Oxygen Species in Osteosarcoma and Potential Treatment Applications.Cells · 2019Article
- The oxidoreductase p66Shc acts as tumor suppressor in BRAFV600E-transformed cells.Molecular oncology · 2018Article
- Mcl-1 regulates reactive oxygen species via NOX4 during chemotherapy-induced senescence.Oncotarget · 2017Article
- Novel Insights into the PKCβ-dependent Regulation of the Oxidoreductase p66Shc.The Journal of biological chemistry · 2016Article
- cJun N-terminal kinase (JNK) phosphorylation of serine 36 is critical for p66Shc activation.Scientific reports · 2016Article
- C-Raf deficiency leads to hearing loss and increased noise susceptibility.Cellular and molecular life sciences : CMLS · 2015Article
- RNA-seq based transcriptome analysis of hepatitis E virus (HEV) and hepatitis B virus (HBV) replicon transfected Huh-7 cells.PloS one · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
We have shown previously that mitochondrial ROS production is essential to turn growth factor (GF) removal into cell death. Activated RAF, AKT, Bcl-2 and antioxidants protected equally well against ROS accumulation and subsequent death. Here we investigated whether protection by survival signaling and antioxidants utilizes shared or distinct targets. Using serum deprivation from NIH 3T3 fibroblasts and IL-3 withdrawal from promyeloid 32D cells, we showed that pro-survival signaling by activated RAF but not AKT prevented the decline in Mcl-1 following GF abrogation. GF starvation increased levels of Bim in both model systems, which was prevented by RAF in 32D cells but not in NIH 3T3 fibroblasts. RAF and AKT suppressed activation and mitochondrial translocation of BAX. Also, antioxidant treatment efficiently prevented BAX activation and death of 32D cells but showed little effect on its mitochondrial translocation. No significant impact of antioxidant treatment on Bim or Mcl-1 expression was observed. ROS produced during GF abrogation also did not alter the activity of intracellular signaling pathways, which have been implicated previously in cell killing by pro-oxidants. Together these data suggest Bcl-2 family proteins as convergence point for RAF and ROS in life and death decisions.
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