ArticleiScience2025
Developing therapeutic strategies to target MCL1 and BCLXL in lethal prostate cancer.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
27 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeting anti-apoptotic BCL2 family proteins is an attractive therapeutic strategy to drive prostate cancer (PCa) cell death. Here, we show that MCL1 is highly expressed in castration-resistant PCa, associating with worse clinical outcome. We demonstrate that targeting MCL1 with BH3 mimetics triggers apoptotic cell death in a subset of PCa cell line models. Furthermore, siRNA targeting of UCHL3, a deubiquitinating enzyme, downregulates MCL1 expression to synergize with BCLXL blockade; however, its impact on MCL1 is driven through an off-target effect, raising an important methodological consideration when studying MCL1 biology. Finally, we demonstrate that co-targeting MCL1 and BCLXL in patient-derived and mouse PCa models drives apoptotic PCa cell death. Taken together, targeting the intrinsic apoptosis pathway remains an attractive therapeutic strategy for lethal PCa. Future studies should focus on identifying strategies and technologies that can deliver cancer specific kill, to improve the outcome for men with this lethal disease.
Indexed as
Identifiers
What Socratic 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 Socratic graph.