ArticleNature communications2021
Opposing transcriptional programs of KLF5 and AR emerge during therapy for advanced prostate cancer.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- Recurrent mechanisms of biallelic epigenetic inactivation reveal new putative tumour suppressor genes in prostate cancer.Nature communications · 2026Article
- ERBB2 as a Prognostic Biomarker in Prostate Cancer: Integration of Single-Cell Transcriptomics, Deep Learning, and Immunohistochemical Validation.Biochemical genetics · 2026Article
- 3D genome architecture and epigenetic regulation of lineage identity in advanced prostate cancer.Endocrinology · 2026Review
- CREB5 regulates stem cell-like transcriptional programs to enhance tumor progression in prostate cancer.Oncotarget · 2026Article
- EZH2 Suppression Diversifies Prostate Cancer Lineage Variant Evolution and Lacks Efficacy in Inhibiting Disease Progression.Cancer research · 2026Article
- Proteomic Profiling of Extracellular Vesicles Distinguishes Prostate Cancer Molecular Subtypes.Journal of extracellular vesicles · 2025Article
- Divergent FOXA1 mutations drive prostate tumorigenesis and therapy-resistant cellular plasticity.Science (New York, N.Y.) · 2025Article
- Identification of asporin as a HER3 ligand exposes a therapeutic vulnerability in prostate cancer.JCI insight · 2025Article
- Comparative transcriptomics reveals a mixed basal, club, and hillock epithelial cell identity in castration-resistant prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The miR-1305/KLF5 negative regulatory loop affects pancreatic cancer cell proliferation and apoptosis.Human cell · 2025Article
- Integrated multi-omics assessment of lineage plasticity in a prostate cancer patient with brain and dural metastases.NPJ precision oncology · 2024Article
- An Atlas of Accessible Chromatin in Advanced Prostate Cancer Reveals the Epigenetic Evolution during Tumor Progression.Cancer research · 2024Article
- ONECUT2 acts as a lineage plasticity driver in adenocarcinoma as well as neuroendocrine variants of prostate cancer.Nucleic acids research · 2024Article
- Computer-aided drug discovery strategies for novel therapeutics for prostate cancer leveraging next-generating sequencing data.Expert opinion on drug discovery · 2024Review
- Treatment-induced stemness and lineage plasticity in driving prostate cancer therapy resistance.Cancer heterogeneity and plasticity · 2024Article
- Prostate cancer genetic risk and associated aggressive disease in men of African ancestry.Nature communications · 2023Article
- ONECUT2 Activates Diverse Resistance Drivers of Androgen Receptor-Independent Heterogeneity in Prostate Cancer.bioRxiv : the preprint server for biology · 2023Article
- The Genomic and Epigenomic Landscape of Double-Negative Metastatic Prostate Cancer.Cancer research · 2023Article
- A CRISPR/Cas9-based kinome screen identifies ErbB signaling as a new regulator of human naïve pluripotency and totipotency.Life medicine · 2023Article
- Basal epithelial cells in prostate development, tumorigenesis, and cancer progression.Cell cycle (Georgetown, Tex.) · 2023Review
Corrections and comments
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Authors and funding
34 authors at 12 institutions in 5 countries.
Funding
Abstract
Endocrine therapies for prostate cancer inhibit the androgen receptor (AR) transcription factor. In most cases, AR activity resumes during therapy and drives progression to castration-resistant prostate cancer (CRPC). However, therapy can also promote lineage plasticity and select for AR-independent phenotypes that are uniformly lethal. Here, we demonstrate the stem cell transcription factor Krüppel-like factor 5 (KLF5) is low or absent in prostate cancers prior to endocrine therapy, but induced in a subset of CRPC, including CRPC displaying lineage plasticity. KLF5 and AR physically interact on chromatin and drive opposing transcriptional programs, with KLF5 promoting cellular migration, anchorage-independent growth, and basal epithelial cell phenotypes. We identify ERBB2 as a point of transcriptional convergence displaying activation by KLF5 and repression by AR. ERBB2 inhibitors preferentially block KLF5-driven oncogenic phenotypes. These findings implicate KLF5 as an oncogene that can be upregulated in CRPC to oppose AR activities and promote lineage plasticity.
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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 Socratic graph.