ArticleProceedings of the National Academy of Sciences of the United States of America2004
Transcriptional switch by activating transcription factor 2-derived peptide sensitizes melanoma cells to apoptosis and inhibits their tumorigenicity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 55 citations in OpenAlex.
- Structural and functional characterisation of ATF2 nuclear import reveals paralogue-selective importin-α recognition and a non-canonical NLS formed in trans.Life science alliance · 2026Article
- Therapeutic targeting of anoikis resistance in cutaneous melanoma metastasis.Frontiers in cell and developmental biology · 2023Review
- Emerging roles of activating transcription factor (ATF) family members in tumourigenesis and immunity: Implications in cancer immunotherapy.Genes & diseases · 2022Review
- Overexpression of Activating Transcription Factor-2 (ATF-2) Activates Wnt/CaDisease markers · 2022Article
- Review
- Rsu1-dependent control of PTEN expression is regulated via ATF2 and cJun.Journal of cell communication and signaling · 2019Article
- Infected erythrocyte-derived extracellular vesicles alter vascular function via regulatory Ago2-miRNA complexes in malaria.Nature communications · 2016Article
- ATF2 predicts poor prognosis and promotes malignant phenotypes in renal cell carcinoma.Journal of experimental & clinical cancer research : CR · 2016Article
- A Transcriptionally Inactive ATF2 Variant Drives Melanomagenesis.Cell reports · 2016Article
- The transcription factor ATF2 promotes melanoma metastasis by suppressing protein fucosylation.Science signaling · 2015Article
- Article
- Mitochondrial ATF2 translocation contributes to apoptosis induction and BRAF inhibitor resistance in melanoma through the interaction of Bim with VDAC1.Oncotarget · 2015Article
- The intracellular domain of cell adhesion molecule 1 is present in emphysematous lungs and induces lung epithelial cell apoptosis.Journal of biomedical science · 2015Article
- Bim and VDAC1 are hierarchically essential for mitochondrial ATF2 mediated cell death.Cancer cell international · 2015Article
- AP-1-mediated expression of brain-specific class IVa β-tubulin in P19 embryonal carcinoma cells.The Journal of veterinary medical science · 2014Article
- ATF2 knockdown reinforces oxidative stress-induced apoptosis in TE7 cancer cells.Journal of cellular and molecular medicine · 2013Article
- Degradation of newly synthesized polypeptides by ribosome-associated RACK1/c-Jun N-terminal kinase/eukaryotic elongation factor 1A2 complex.Molecular and cellular biology · 2013Article
- Inhibition of melanoma growth by small molecules that promote the mitochondrial localization of ATF2.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Article
- ATF2 - at the crossroad of nuclear and cytosolic functions.Journal of cell science · 2012Article
- Subtype and pathway specific responses to anticancer compounds in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The notorious resistance of melanoma cells to drug treatment can be overcome by expression of a 50-aa peptide derived from activating transcription factor 2 (ATF2(50-100)). Here we demonstrate that ATF2(50-100) induced apoptosis by sequestering ATF2 to the cytoplasm, thereby inhibiting its transcriptional activities. Furthermore, ATF2(50-100) binds to c-Jun N-terminal kinase (JNK) and increases its activity. Mutation within ATF2(50-100) that impairs association with JNK and the inhibition of JNK or c-Jun expression by RNA interference (RNAi) reduces the degree of ATF2(50-100)-induced apoptosis. In contrast, TAM67, a dominant negative of the Jun family of transcription factors, or JunD RNAi attenuates sensitization of melanoma cells expressing ATF2(50-100) to apoptosis after treatment with anisomycin, which is used as a model drug. Mutations within the JNK binding region of ATF2(50-100) or expression of TAM67 or JunD RNAi attenuates inhibition of melanoma's tumorigenicity by ATF2(50-100). We conclude that inhibition of ATF2 in concert with increased JNK/Jun and JunD activities is central for the sensitization of melanoma cells to apoptosis and inhibition of their tumorigenicity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.