The castration-resistant prostate cancer-associated SNP rs11067228 facilitates neuroendocrine differentiation through an enhancer-mediated chromatin interaction with SRRM4.

doi:10.7150/ijbs.124731

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

The castration-resistant prostate cancer-associated SNP rs11067228 facilitates neuroendocrine differentiation through an enhancer-mediated chromatin interaction with SRRM4.

International journal of biological sciences - 1 Jan 2026

Jiang Yuan, Zhao Zhenhao, Li Peng, Su Guangsong, Qian Yuyang, Zhao Yuting, Wang Bo, Bai Yunlong, Zhang Lei, Zhao Zhongfang, Shi Jiandang, Lu Wange

Abstract excerpt

Neuroendocrine prostate cancer is an aggressive disease characterized by early metastasis, drug resistance and poor prognosis. Genome-wide association studies (GWAS) previously identified numerous single nucleotide polymorphisms (SNPs) associated with prostate cancer. SNP rs11067228 as a significant variant associated with castration-resistant metastasis (CM) in prostate cancer (PCa). However, mechanisms...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Differentiation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Line, Tumor

Share to Chromatin

Share to Enhancer Elements, Genetic

Share to Gene Expression Regulation, Neoplastic

Share to Mice

Share to Nerve Tissue Proteins

Share to Prostatic Neoplasms, Castration-Resistant

Source

Open in PubMed Open full text

Identifiers

PMID: 41608622
DOI: 10.7150/ijbs.124731
PMCID: PMC12837743

Genes

SRRM4
SOX4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The castration-resistant prostate cancer-associated SNP rs11067228 facilitates neuroendocrine differentiation through an enhancer-mediated chromatin interaction with SRRM4.PMID 41608622Read ↗

RNA Splicing Factors SRRM3 and SRRM4 Distinguish Molecular Phenotypes of Castration-Resistant Neuroendocrine Prostate CancerSemantic proximity Read ↗

Establishment of a neuroendocrine prostate cancer model driven by the RNA splicing factor SRRM4Semantic proximity Read ↗

A novel mechanism of SRRM4 in promoting neuroendocrine prostate cancer development via a pluripotency gene networkSemantic proximity Read ↗

Dysregulated Alternative Splicing Landscape Identifies Intron Retention as a Hallmark and Spliceosome as a Therapeutic Vulnerability in Aggressive Prostate CancerSemantic proximity Read ↗

Molecular profiling stratifies diverse phenotypes of treatment-refractory metastatic castration-resistant prostate cancerSemantic proximity Read ↗

Alternative splicing of LSD1+8a in neuroendocrine prostate cancer is mediated by SRRM4Semantic proximity Read ↗

Genomic and transcriptomic features of androgen receptor signaling inhibitor resistance in metastatic castration-resistant prostate cancerSemantic proximity Read ↗

The splicing factor SRSF6 regulates AR activity and represents a potential therapeutic target in prostate cancerSemantic proximity Read ↗

RNA splicing and splicing regulator changes in prostate cancer pathologySemantic proximity Read ↗

The SOX4/miR-17-92/RB1 Axis Promotes Prostate Cancer ProgressionSemantic proximity Read ↗

An enhancer from the 8q24 prostate cancer risk region is sufficient to direct reporter gene expression to a subset of prostate stem-like epithelial cells in transgenic mice.Semantic proximity Read ↗

Integrative identification of non-coding regulatory regions driving metastatic prostate cancer.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.