ArticleCancer research2026
MECOM Function Is Critical for AR-Driven Treatment-Resistant Prostate Cancer.
Article in Cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- The oncogenic role of ecotropic viral integration site 1 in hematological malignancies: mechanisms of activation and leukemogenesis.Frontiers in immunology · 2026Review
- Androgen receptor reactivation in castration-resistant prostate cancer: mechanisms, epigenetic adaptation, and therapeutic vulnerabilities.Frontiers in oncology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
Abstract
Reprogramming of the androgen receptor (AR) cistrome is associated with prostate cancer progression, and advanced castration-resistant prostate cancers (CRPC) tend to rely on reprogrammed/noncanonical AR signaling that remains active under treatment with AR signaling inhibitors (ARSI). In this study, we identified ecotropic viral integration site 1 (EVI1), an oncogenic nuclear transcription factor (TF) encoded by MECOM, as an AR-recruited coactivator of noncanonical signaling. In prostate cancer, MECOM was exclusively overexpressed in both CRPC and enzalutamide-resistant CRPC and interacted with AR in the nucleus. MECOM depletion in prostate cancer cells decreased proliferation, altered cell survival transcriptional programs, and reduced the number of super-enhancers (SE), leading to a dynamic change in the SE landscape and a decrease in the expression of SE-regulated oncogenic TFs, along with increased proapoptotic signatures. Notably, cells overexpressing MECOM and its protein, EVI1, were susceptible to PARP inhibitors (PARPi) regardless of their DNA damage response or homologous recombination repair (HRR) gene mutation status. These insights reveal the crucial role of EVI1 in regulating cell survival within the context of an AR-reprogrammed chromatin landscape. More importantly, the findings suggest that MECOM overexpression may be another biomarker that could significantly broaden the use of PARPis beyond those with HRR gene mutations. SIGNIFICANCE: MECOM is a driver of androgen receptor inhibitor resistance in castrate-resistant prostate cancer that promotes susceptibility to PARP inhibition, positioning MECOM as a biomarker in patients without homologous recombination repair gene mutations.
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.