ArticleCell chemical biology2024
PIM1 targeted degradation prevents the emergence of chemoresistance in prostate cancer.
Article in Cell chemical biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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
9 citing papers in PubMed, 14 citations in OpenAlex.
- Apatinib resistance mediated by IRF9 nuclear translocation in head and neck squamous cell carcinoma.iScience · 2026Article
- Exploring PIM1 Kinase as a Therapeutic Target: Mechanisms and Strategies in Cancer Treatment.International journal of molecular sciences · 2026Review
- Review
- RuPHOTACs Provide Photocontrol Over Protein Degradation with Optimized Properties for Biological Applications.Research square · 2026Article
- PIM kinase inhibition attenuates pro-tumoral and immunosuppressive functions of macrophages in classic Hodgkin lymphoma.Cell death & disease · 2025Article
- In Silico Identification of circPIM1/miR-16-5p/miR-195-5p/PIM1 Feed-Forward Loop in Recurrent Grade 2 Meningioma.International journal of molecular sciences · 2025Article
- Inhibition of PIM Kinase in Tumor-Associated Macrophages Suppresses Inflammasome Activation and Sensitizes Prostate Cancer to Immunotherapy.Cancer immunology research · 2025Article
- Epigenetic underpinnings of tumor-immune dynamics in prostate cancer immune suppression.Trends in cancer · 2024Review
- Defeating kinases that promote tumorigenesis through non-catalytic functions with PROTACs - PIM kinase as an example.Expert opinion on therapeutic targetsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 2 countries.
Funding
Abstract
PIM kinases have important pro-tumorigenic roles and mediate several oncogenic traits, including cell proliferation, survival, and chemotherapeutic resistance. As a result, multiple PIM inhibitors have been pursued as investigational new drugs in cancer; however, response to PIM inhibitors in solid tumors has fallen short of expectations. We found that inhibition of PIM kinase activity stabilizes protein levels of all three PIM isoforms (PIM1/2/3), and this can promote resistance to PIM inhibitors and chemotherapy. To overcome this effect, we designed PIM proteolysis targeting chimeras (PROTACs) to target PIM for degradation. PIM PROTACs effectively downmodulated PIM levels through the ubiquitin-proteasome pathway. Importantly, degradation of PIM kinases was more potent than inhibition of catalytic activity at inducing apoptosis in prostate cancer cell line models. In conclusion, we provide evidence of the advantages of degrading PIM kinases versus inhibiting their catalytic activity to target the oncogenic functions of PIM kinases.
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.