ArticleThe Journal of biological chemistry2011
BCL-2 is a downstream target of ATF5 that mediates the prosurvival function of ATF5 in a cell type-dependent manner.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 85 citations in OpenAlex.
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- Decreased ATF5 level contributes to improved mitochondrial function in oocytes exposed to vitrification stress.Frontiers in cell and developmental biology · 2024Article
- Dpep Inhibits Cancer Cell Growth and Survival via Shared and Context-Dependent Transcriptome Perturbations.Cancers · 2023Article
- Transcriptome-wide association study identifies novel candidate susceptibility genes for migraine.HGG advances · 2023Article
- Review
- The Journey of Mitochondrial Protein Import and the Roadmap to Follow.International journal of molecular sciences · 2023Review
- ATF5 promotes malignant T cell survival through the PI3K/AKT/mTOR pathway in cutaneous T cell lymphoma.Frontiers in immunology · 2023Article
- Basic Leucine Zipper Transcription Factors as Important Regulators of Leydig Cells' Functions.International journal of molecular sciences · 2022Review
- Mitochondria: intracellular sentinels of infections.Medical microbiology and immunology · 2022Review
- The mitochondrial unfolded protein response (UPRJournal of hematology & oncology · 2022Review
- Emerging roles of activating transcription factor (ATF) family members in tumourigenesis and immunity: Implications in cancer immunotherapy.Genes & diseases · 2022Review
- The Basis and Advances in Clinical Application of Cytomegalovirus-Specific Cytotoxic T Cell Immunotherapy for Glioblastoma Multiforme.Frontiers in oncology · 2022Review
- EBF1 is expressed in pericytes and contributes to pericyte cell commitment.Histochemistry and cell biology · 2021Article
- Influence of genetic variants in asparaginase pathway on the susceptibility to asparaginase-related toxicity and patients' outcome in childhood acute lymphoblastic leukemia.Cancer chemotherapy and pharmacology · 2021Article
- Cell-Penetrating CEBPB and CEBPD Leucine Zipper Decoys as Broadly Acting Anti-Cancer Agents.Cancers · 2021Article
- Targeting the Integrated Stress Response in Cancer Therapy.Frontiers in pharmacology · 2021Review
- Systems Biomedicine of Primary and Metastatic Colorectal Cancer Reveals Potential Therapeutic Targets.Frontiers in oncology · 2021Article
- Expression patterns of activating transcription factor 5 (atf5a and atf5b) in zebrafish.Gene expression patterns : GEP · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ATF5 loss of function has been shown previously to cause apoptotic cell death in glioblastoma and breast cancer cells but not in non-transformed astrocytes and human breast epithelial cells. The mechanism for the cell type-dependent survival function of ATF5 is unknown. We report here that the anti-apoptotic factor BCL-2 is a downstream target of ATF5 that mediates the prosurvival function of ATF5 in C6 glioma cells and MCF-7 breast cancer cells. ATF5 binds to an ATF5-specific regulatory element that is downstream of and adjacent to the negative regulatory element in the BCL-2 P2 promoter, stimulating BCL-2 expression. Highlighting the critical role of BCL-2 in ATF5-dependent cancer cell survival, expression of BCL-2 blocks death of C6 and MCF-7 cells induced by dominant-negative ATF5, and depletion of BCL-2 impairs ATF5-promoted cell survival. Moreover, we found that BCL-2 expression is not regulated by ATF5 in non-transformed rat astrocytes, mouse embryonic fibroblasts, and human breast epithelial cells, where expression of BCL-2 but not ATF5 is required for cell survival. These findings identify BCL-2 as an essential mediator for the cancer-specific cell survival function of ATF5 in glioblastoma and breast cancer cells and provide direct evidence that the cell type-specific function of ATF5 derives from differential regulation of downstream targets by ATF5 in different types of cells.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.