Evidence map›Paper›PMID 42218299›Full record

ArticleOncogene2026

Histone methyltransferase KMT2D promotes castration-resistant prostate cancer progression by reactivating AR through FOXA1.

Mayao Luo, Chenwei Wu, Manli Zhou, Rui Liu, Yifan Zhang, Yadong Li, Yuanpeng Liao, Xin Huang, Chuance Du, Shidong Lv and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Mayao Luo *Department of Urology, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Chenwei Wu *Department of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Manli ZhouDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Rui LiuSouthern Medical University, Guangdong, China.
Yifan ZhangDepartment of Urology, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0002-4641-3412
Yadong LiDepartment of Urology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Yuanpeng LiaoDepartment of Urology, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China.
Xin HuangDepartment of Urology, Ganzhou Hospital-Nanfang Hospital, Southern Medical University, Ganzhou, Jiangxi, China.
Chuance DuDepartment of Urology, Ganzhou Hospital-Nanfang Hospital, Southern Medical University, Ganzhou, Jiangxi, China. duchuance@126.com.
Shidong LvDepartment of Urology, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China. lsd990@smu.edu.cn.
Qiang WeiDepartment of Urology, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, Guangzhou, Guangdong, China. qwei@smu.edu.cn.ORCID http://orcid.org/0000-0002-6875-7697

Funding

China Postdoctoral Science Foundation 2025M781946National Natural Science Foundation of China (National Science Foundation of China) 82472756,82103276Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2023A1515010321Natural Science Foundation of Guangdong Province (Guangdong Natural Science Foundation) 2024A1515010331Natural Science Foundation of Jiangxi Province (Jiangxi Province Natural Science Foundation) 20224ACB206007
6 · The paper itself

Abstract

Prostate cancer (PCa) progression, particularly to castration-resistant prostate cancer (CRPC), is driven by androgen receptor (AR) reactivation and epigenetic alterations. Here, we identify lysine methyltransferase 2D (KMT2D) as a critical epigenetic oncogene in PCa. KMT2D expression is elevated in PCa and correlates with poor prognosis. Mechanistically, KMT2D facilitates AR signaling by recruiting the pioneer factor FOXA1 to AR-specific enhancers, promoting chromatin accessibility and activating AR target genes. FOXA1 mutations impair this regulation, demonstrating their functional interplay. Furthermore, KMT2D-FOXA1-AR axis modulates ketone body metabolism via transcriptional control of HMGCS2, supporting tumor growth. Pharmacological inhibition of UTX, a COMPASS complex demethylase essential for KMT2D function, disrupts H3K4me1 deposition and suppresses AR signaling and tumor proliferation. Altogether, we characterize KMT2D as a key driver of AR-dependent PCa progression and propose UTX inhibition as a promising therapeutic strategy.

Indexed as

DNA-Binding ProteinsHepatocyte Nuclear Factor 3-alphaNeoplasm ProteinsProstatic Neoplasms, Castration-ResistantReceptors, AndrogenAnimalsCell Line, TumorCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHistone DemethylasesHumansMaleMiceSignal TransductionAR protein, humanDNA-Binding ProteinsFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaHistone DemethylasesKMT2D protein, humanNeoplasm ProteinsReceptors, Androgen

Identifiers

PMID42218299

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.