ArticleThe Journal of biological chemistry2008
Transcriptional repression of the prosurvival endoplasmic reticulum chaperone GRP78/BIP by E2F1.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 50 citations in OpenAlex.
- LINC00629 protects osteosarcoma cell from ER stress-induced apoptosis and facilitates tumour progression by elevating KLF4 stability.Journal of experimental & clinical cancer research : CR · 2022Article
- Ribosomal protein L5 (RPL5)/ E2F transcription factor 1 (E2F1) signaling suppresses breast cancer progression via regulating endoplasmic reticulum stress and autophagy.Bioengineered · 2022Article
- Article
- Dermatan Sulfate Is a Potential Regulator of IgHFrontiers in immunology · 2021Article
- Mechanism of inositol-requiring enzyme 1-alpha inhibition in endoplasmic reticulum stress and apoptosis in ovarian cancer cells.Journal of cell communication and signaling · 2020Article
- Endoplasmic reticulum stress is transmissible in vitro between cells of the central nervous system.Journal of neurochemistry · 2019Article
- Antimetastatic Effect of Fucoidan-Sargassum against Liver Cancer Cell Invadopodia Formation via Targeting Integrin αVβ3 and Mediating αVβ3/Src/E2F1 Signaling.Journal of Cancer · 2019Article
- ATF4 destabilizes RET through nonclassical GRP78 inhibition to enhance chemosensitivity to bortezomib in human osteosarcoma.Theranostics · 2019Article
- TM7SF3, a novel p53-regulated homeostatic factor, attenuates cellular stress and the subsequent induction of the unfolded protein response.Cell death and differentiation · 2017Article
- The downregulation of the RNA-binding protein Staufen2 in response to DNA damage promotes apoptosis.Nucleic acids research · 2016Article
- Epigenetic factor EPC1 is a master regulator of DNA damage response by interacting with E2F1 to silence death and activate metastasis-related gene signatures.Nucleic acids research · 2016Article
- Article
- Lipase maturation factor 1 (lmf1) is induced by endoplasmic reticulum stress through activating transcription factor 6α (Atf6α) signaling.The Journal of biological chemistry · 2014Article
- E2F2 and CREB cooperatively regulate transcriptional activity of cell cycle genes.Nucleic acids research · 2013Article
- Gene regulatory network of unfolded protein response genes in endoplasmic reticulum stress.Cell stress & chaperones · 2013Article
- Rb/E2F1 regulates the innate immune receptor Toll-like receptor 3 in epithelial cells.Molecular and cellular biology · 2012Article
- Review
- Article
- Conserved RB functions in development and tumor suppression.Protein & cell · 2011Review
- Targeting Rb inactivation in cancers by synthetic lethality.American journal of cancer research · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endoplasmic reticulum chaperone GRP78/BIP plays a central role in the prosurvival machinery, and its enhanced expression has been implicated in drug resistance, carcinogenesis, and metastasis. E2F1, as part of an antitumor safeguard mechanism, promotes apoptosis regardless of functional p53. Using cells that are defective in p53, we show that E2F1 represses GRP78/BIP at the transcriptional level, and this requires its DNA binding domain. Analysis of human GRP78/BIP promoter reporter constructs revealed that the region between -371 and -109 of the proximal promoter contains major E2F1-responsive elements. Toward understanding the underlying mechanism of this regulation, we performed chromatin immunoprecipitation and gel shift assays, demonstrating that E2F1 directly binds to GC-rich regions in the distal GC-box and endoplasmic reticulum stress response element -126 by interfering with the binding of positive regulatory proteins Sp1 and TFII-I of the ER stress response element-binding factor complex. We further show that TFII-I, which is required for optimal stress induction of GRP78/BIP, is suppressed by E2F1 on the protein level. Finally, our studies suggest a molecular link between the inhibition of GRP78/BIP and E2F1-mediated chemosensitization of tumor cells, underscoring its relevance for cancer treatment. Together, the data provide a new mechanism for the incompletely understood tumor suppressor function of E2F1.
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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.