ArticleAmerican journal of cancer research2024
PGC1α as a downstream effector of KDM5B promotes the progression of androgen receptor-positive and androgen receptor-negative prostate cancers.
Article in American journal of cancer research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- KDM5B-driven glucose metabolic reprogramming promotes enzalutamide resistance in prostate cancer via the lactate/hnRNPA1 lactylation/AR-V7 axis.Molecular cancer · 2026Article
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6 authors.
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Abstract
PPARγ coactivator-1α (PGC1α), as a co-activator, is known to optimize the action of several transcription factors, including androgen receptor (AR). However, the precise functions of PGC1α in prostate cancer, particularly those via the non-AR pathways, remain poorly understood. Meanwhile, our bioinformatics search suggested that PGC1α could be a direct downstream target of lysine-specific demethylase 5B (KDM5B/JARID1B/PLU1). We herein aimed to investigate how PGC1α induced prostate cancer outgrowth. Immunohistochemistry in radical prostatectomy specimens showed that the levels of PGC1α expression were significantly higher in prostatic adenocarcinoma [H-score (mean ± SD): 179.0 ± 111.6] than in adjacent normal-appearing tissue (16.7 ± 29.9,
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