ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2021
Co-Targeting Plk1 and DNMT3a in Advanced Prostate Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 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
10 citing papers in PubMed, 17 citations in OpenAlex.
- The Quartet of Core Oncogenic Drivers in Neuroendocrine Prostate Cancer: Multi-Omics Dataset Integration to Forge a Translational Link Between Biology and Precision Therapy.International journal of biological sciences · 2026Review
- PLK1 overexpression as a dual-role biomarker and therapeutic vulnerability in pulmonary adenocarcinoma.PeerJ · 2026Article
- The Role of DNA Methyltransferases in Urinary System Diseases.Cancer innovation · 2025Review
- Targeting RPS6KC1 to overcome enzalutamide resistance in prostate cancer.Biomarker research · 2025Article
- DiCE: differential centrality-ensemble analysis based on gene expression profiles and protein-protein interaction network.Nucleic acids research · 2025Article
- Elevating PLK1 overcomes BETi resistance in prostate cancer via triggering BRD4 phosphorylation-dependent degradation in mitosis.Cell reports · 2024Article
- TransGEM: a molecule generation model based on Transformer with gene expression data.Bioinformatics (Oxford, England) · 2024Article
- PLK1: A Promising Therapeutic Target for Prostate Cancer Treatment.Serican journal of medicine · 2024Article
- Emerging role of exosomes in cancer progression and tumor microenvironment remodeling.Journal of hematology & oncology · 2022Review
- Co-Targeting Plk1 and DNMT3a in Advanced Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
Because there is no effective treatment for late-stage prostate cancer (PCa) at this moment, identifying novel targets for therapy of advanced PCa is urgently needed. A new network-based systems biology approach, XDeath, is developed to detect crosstalk of signaling pathways associated with PCa progression. This unique integrated network merges gene causal regulation networks and protein-protein interactions to identify novel co-targets for PCa treatment. The results show that polo-like kinase 1 (Plk1) and DNA methyltransferase 3A (DNMT3a)-related signaling pathways are robustly enhanced during PCa progression and together they regulate autophagy as a common death mode. Mechanistically, it is shown that Plk1 phosphorylation of DNMT3a leads to its degradation in mitosis and that DNMT3a represses Plk1 transcription to inhibit autophagy in interphase, suggesting a negative feedback loop between these two proteins. Finally, a combination of the DNMT inhibitor 5-Aza-2'-deoxycytidine (5-Aza) with inhibition of Plk1 suppresses PCa synergistically.
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.