ArticleCancer research2017
A Naturally Generated Decoy of the Prostate Apoptosis Response-4 Protein Overcomes Therapy Resistance in Tumors.
Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 38 citations in OpenAlex.
- Fbxo45 facilitates the malignant progression of breast cancer by targeting Bim for ubiquitination and degradation.BMC cancer · 2024Article
- Therapeutic Potential of Decoys for Prostate Cancers: A Review of Recent Updates.Current medicinal chemistry · 2024Review
- Crizotinib induces Par-4 secretion from normal cells and GRP78 expression on the cancer cell surface for selective tumor growth inhibition.American journal of cancer research · 2023Article
- Potent Synergistic Effect on C-Myc-Driven Colorectal Cancers Using a Novel Indole-Substituted Quinoline with a Plk1 Inhibitor.Molecular cancer therapeutics · 2021Article
- Structural Analysis of the cl-Par-4 Tumor Suppressor as a Function of Ionic Environment.Biomolecules · 2021Article
- Post-Translational Modifications That Drive Prostate Cancer Progression.Biomolecules · 2021Review
- Prostate apoptosis response-4 and tumor suppression: it's not just about apoptosis anymore.Cell death & disease · 2021Review
- Peptidome characterization of ovarian cancer serum and the identification of tumor suppressive peptide ZYXAnnals of translational medicine · 2020Article
- FBXO45 is a potential therapeutic target for cancer therapy.Cell death discovery · 2020Review
- PAR-4 overcomes chemo-resistance in breast cancer cells by antagonizing cIAP1.Scientific reports · 2019Article
- pH-Induced Folding of the Caspase-Cleaved Par-4 Tumor Suppressor: Evidence of Structure Outside of the Coiled Coil Domain.Biomolecules · 2018Article
- PAM forms an atypical SCF ubiquitin ligase complex that ubiquitinates and degrades NMNAT2.The Journal of biological chemistry · 2018Article
- Identification of aberrantly expressed F-box proteins in squamous-cell lung carcinoma.Journal of cancer research and clinical oncology · 2018Article
- Foxo-dependent Par-4 Upregulation Prevents Long-term Survival of Residual Cells Following PI3K-Akt Inhibition.Molecular cancer research : MCR · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Primary tumors are often heterogeneous, composed of therapy-sensitive and emerging therapy-resistant cancer cells. Interestingly, treatment of therapy-sensitive tumors in heterogeneous tumor microenvironments results in apoptosis of therapy-resistant tumors. In this study, we identify a prostate apoptosis response-4 (Par-4) amino-terminal fragment (PAF) that is released by diverse therapy-sensitive cancer cells following therapy-induced caspase cleavage of the tumor suppressor Par-4 protein. PAF caused apoptosis in cancer cells resistant to therapy and inhibited tumor growth. A VASA segment of Par-4 mediated its binding and degradation by the ubiquitin ligase Fbxo45, resulting in loss of Par-4 proapoptotic function. Conversely, PAF, which contains this VASA segment, competitively bound to Fbxo45 and rescued Par-4-mediated induction of cancer cell-specific apoptosis. Collectively, our findings identify a molecular decoy naturally generated during apoptosis that inhibits a ubiquitin ligase to overcome therapy resistance in tumors.
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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.