ArticleOncogene2013
The ubiquitin ligase CHIP regulates c-Myc stability and transcriptional activity.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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Who cites it
93 citing papers in PubMed, 171 citations in OpenAlex.
- STUB1 downregulates TOP2A through a dual mechanism of ubiquitination and FOXM1-mediated transcription repression, suppressing breast cancer growth and enhancing sensitivity to chemotherapy.Cellular & molecular biology letters · 2026Article
- CHIP and aging: a key regulator of proteostasis and cellular senescence.Biogerontology · 2025Review
- TACC3 enhances glycolysis in bladder cancer cells through inducing acetylation of c-Myc.Cell death & disease · 2025Article
- Review
- The RING-type E3 ligase RIE1 sustains leaf longevity by specifically targeting AtACS7 to fine-tune ethylene production inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Proteostasis perturbation of N-Myc leveraging HSP70 mediated protein turnover improves treatment of neuroendocrine prostate cancer.Nature communications · 2024Article
- CHIP promotes CAD ubiquitination and degradation to suppress the proliferation and colony formation of glioblastoma cells.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- New insights in ubiquitin-dependent Wnt receptor regulation in tumorigenesis.In vitro cellular & developmental biology. Animal · 2024Review
- Review
- The HSP90-MYC-CDK9 network drives therapeutic resistance in mantle cell lymphoma.Experimental hematology & oncology · 2024Article
- USP43 stabilizes c-Myc to promote glycolysis and metastasis in bladder cancer.Cell death & disease · 2024Article
- Imatinib induces ferroptosis in gastrointestinal stromal tumors by promoting STUB1-mediated GPX4 ubiquitination.Cell death & disease · 2023Article
- Akt Is Controlled by Bag5 through a Monoubiquitination to Polyubiquitination Switch.International journal of molecular sciences · 2023Article
- Histone demethylase KDM4B accelerates the progression of glioblastoma via the epigenetic regulation of MYC stability.Clinical epigenetics · 2023Article
- Mitoribosomal synthetic lethality overcomes multidrug resistance in MYC-driven neuroblastoma.Cell death & disease · 2023Article
- Control of SOX2 protein stability and tumorigenic activity by E3 ligase CHIP in esophageal cancer cells.Oncogene · 2023Article
- VBP1 negatively regulates CHIP and selectively inhibits the activity of hypoxia-inducible factor (HIF)-1α but not HIF-2α.The Journal of biological chemistry · 2023Article
- DDIAS, DNA damage-induced apoptosis suppressor, is a potential therapeutic target in cancer.Experimental & molecular medicine · 2023Review
- The Ubiquitin-Proteasome System in Tumor Metabolism.Cancers · 2023Review
- The dual role of p63 in cancer.Frontiers in oncology · 2023Review
33 more citing papers are in PubMed but not listed here.
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
c-Myc is a proto-oncogenic transcription factor and its rapid turnover mediated by the ubiquitin-proteasome system is critical for maintaining normal cellular homeostasis. Multiple ubiquitin ligases have been assigned for c-Myc regulation till date. However, the available data suggest for the possible existence of additional E3 ligase(s). Here, we report a new E3 ligase for c-Myc, the carboxyl terminus of Hsc70-interacting protein or CHIP, which is a chaperone-associated Ubox-containing E3 ligase. In this report, we show that CHIP interacts and ubiquitinates c-Myc, thus targeting it for proteasome-mediated degradation. Overexpression of CHIP could accelerate the turnover rate of c-Myc protein. Conversely, knockdown of CHIP by RNAi stabilizes endogenous c-Myc. The interaction between CHIP and c-Myc depends on the N-terminally located tetratricopeptide repeats of CHIP, which has been implicated as a chaperone-binding motif. Inhibition of Hsp90 chaperone activity by 17-N-allylamino-17-demethoxygeldanamycin reduces c-Myc protein level. We found that the association between CHIP and c-Myc is dependent on the chaperones; particularly Hsp70. CHIP antagonizes the transcriptional activity of c-Myc and decreases the abundance of the transcripts of its target genes. Overall, CHIP-knockdown increases malignant behavior of C6 glioma cells. To the best of our knowledge, this is the first report of c-Myc being regulated by a bona-fide chaperone-associated E3 ligase in HEK293 as well as glioma cells. Because CHIP has been reported earlier to be negatively regulating Akt1, BCR-ABL and hTERT, and now c-Myc, the present study may strengthen the view that CHIP acts as a tumor suppressor.
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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.