ArticleBiomedicines2022
Androgen-Independent Prostate Cancer Is Sensitive to CDC42-PAK7 Kinase Inhibition.
Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 15 citations in OpenAlex.
- Genome-wide association study identifies novel and confirms established loci associated with serum lipids levels in Brazilians.Human genetics · 2026Article
- Obesity Hacks the Brain's Systems for Weight Loss Resistance.Molecular neurobiology · 2025Review
- RNA-binding protein quaking: a multifunctional regulator in tumour progression.Annals of medicine · 2025Review
- Genetic Manipulation in Organoid Models and Their Applications in Central Nervous System Pathologies.Molecular neurobiology · 2025Review
- Rho Small GTPase Family in Androgen-Regulated Prostate Cancer Progression and Metastasis.Cancers · 2025Review
- Gut microbiota and inflammatory bowel disease: mechanisms, clinical implications, and future directions.Molecular biology reports · 2025Review
- Efficacy analysis of 450 nm semiconductor blue laser enucleation of the prostate in treating benign prostatic hyperplasia with urinary retention.Lasers in medical science · 2025Article
- Causal Effects of the Plasma Proteome on Vascular Dementia Risk: A Mendelian Randomization Study with Experimental Validation.Cellular and molecular neurobiology · 2025Article
- Targeting the JAK/STAT3/SOCS signaling pathway in Alzheimer's disease.Inflammopharmacology · 2025Review
- Computer-aided drug discovery strategies for novel therapeutics for prostate cancer leveraging next-generating sequencing data.Expert opinion on drug discovery · 2024Review
- Identification of Molecular Markers Associated with Prostate Cancer Subtypes: An Integrative Bioinformatics Approach.Biomolecules · 2024Article
- The natural history, clinical outcomes, and genotype-phenotype relationship of otoferlin-related hearing loss: a systematic, quantitative literature review.Human genetics · 2023Review
- Associations of the Serum Total Carbon Dioxide Level with Long-Term Clinical Outcomes in Sepsis Survivors.Infectious diseases and therapy · 2023Article
- Clinicopathologic Significance of Quaking Expression in Hepatocellular Carcinoma.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Prostate cancer is a common form of cancer in men, and androgen-deprivation therapy (ADT) is often used as a first-line treatment. However, some patients develop resistance to ADT, and their disease is called castration-resistant prostate cancer (CRPC). Identifying potential therapeutic targets for this aggressive subtype of prostate cancer is crucial. In this study, we show that statins can selectively inhibit the growth of these CRPC tumors that have lost their androgen receptor (AR) and have overexpressed the RNA-binding protein QKI. We found that the repression of microRNA-200 by QKI overexpression promotes the rise of AR-low mesenchymal-like CRPC cells. Using in silico drug/gene perturbation combined screening, we discovered that QKI-overexpressing cancer cells are selectively vulnerable to CDC42-PAK7 inhibition by statins. We also confirmed that PAK7 overexpression is present in prostate cancer that coexists with hyperlipidemia. Our results demonstrate a previously unseen mechanism of action for statins in these QKI-expressing AR-lost CRPCs. This may explain the clinical benefits of the drug and support the development of a biology-driven drug-repurposing clinical trial. This is an important finding that could help improve treatment options for patients with this aggressive form of prostate cancer.
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.