ArticleProceedings of the National Academy of Sciences of the United States of America2014
Prostatic inflammation enhances basal-to-luminal differentiation and accelerates initiation of prostate cancer with a basal cell origin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.
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136 citing papers in PubMed, 186 citations in OpenAlex.
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- ERG Orchestrates a Dedifferentiation-Senescence-Inflammation Triad in Prostate Cancer.Molecular cancer research : MCR · 2026Article
- Prostate Club-like Cells Reveal Context-Dependent Epithelial States in Homeostasis Remodeling and Cancer.Cells · 2026Review
- Cancer stem cell plasticity in shaping drug resistance landscapes in prostate cancer.Journal of advanced research · 2026Review
- Unraveling the microbial landscape in prostate cancer: pathogenesis to therapy.NPJ biofilms and microbiomes · 2026Review
- Prostate Cancer: Etiology, Diagnosis, and Treatment.Serican journal of medicine · 2026Article
- Cellular plasticity and tumor ecosystem dynamics in prostate cancer: insights from single-cell and spatial transcriptomics.American journal of clinical and experimental urology · 2026Review
- Innate immunity and the NF-κB pathway control prostate stem cell plasticity, reprogramming and tumor initiation.Nature cancer · 2025Article
- Link between multiple human papillomavirus 16 and 18 infection and prostate cancer, and relevance of tumor characteristics.Molecular and clinical oncology · 2025Article
- Cell reprogramming in cancer: Interplay of genetic, epigenetic mechanisms, and the tumor microenvironment in carcinogenesis and metastasis.World journal of clinical oncology · 2025Review
- JAK/STAT signaling maintains an intermediate cell population during prostate basal cell fate determination.Nature genetics · 2024Article
- Inflammation impacts androgen receptor signaling in basal prostate stem cells through interleukin 1 receptor antagonist.Communications biology · 2024Article
- The cell fates of intermediate cell population in prostate development.Cell insight · 2024Article
- Prostate cancers with distinct transcriptional programs in Black and White men.Genome medicine · 2024Article
- Evaluation of the clinical application value of cytokine expression profiles in the differential diagnosis of prostate cancer.Cancer immunology, immunotherapy : CII · 2024Article
- Unveiling the Role of Human Papillomavirus in Urogenital Carcinogenesis a Comprehensive Review.Viruses · 2024Review
- The emerging tumor microbe microenvironment: From delineation to multidisciplinary approach-based interventions.Acta pharmaceutica Sinica. B · 2024Review
- Prostate cancer stem cells and their targeted therapies.Frontiers in cell and developmental biology · 2024Review
- Deciphering Urogenital Cancers through Proteomic Biomarkers: A Systematic Review and Meta-Analysis.Cancers · 2023Review
- Inflammation Impacts Androgen Receptor Signaling in Basal Prostate Stem Cells Through Interleukin 1 Receptor Antagonist.Research square · 2023Article
76 more citing papers are in PubMed but not listed here.
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4 authors at 2 institutions in 1 country.
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Abstract
Chronic inflammation has been shown to promote the initiation and progression of diverse malignancies by inducing genetic and epigenetic alterations. In this study, we investigate an alternative mechanism through which inflammation promotes the initiation of prostate cancer. Adult murine prostate epithelia are composed predominantly of basal and luminal cells. Previous studies revealed that the two lineages are largely self-sustained when residing in their native microenvironment. To interrogate whether tissue inflammation alters the differentiation program of basal cells, we conducted lineage tracing of basal cells using a K14-CreER;mTmG model in concert with a murine model of prostatitis induced by infection from the uropathogenic bacteria CP9. We show that acute prostatitis causes tissue damage and creates a tissue microenvironment that induces the differentiation of basal cells into luminal cells, an alteration that rarely occurs under normal physiological conditions. Previously we showed that a mouse model with prostate basal cell-specific deletion of Phosphatase and tensin homolog (K14-CreER;Pten(fl/fl)) develops prostate cancer with a long latency, because disease initiation in this model requires and is limited by the differentiation of transformation-resistant basal cells into transformation-competent luminal cells. Here, we show that CP9-induced prostatitis significantly accelerates the initiation of prostatic intraepithelial neoplasia in this model. Our results demonstrate that inflammation results in a tissue microenvironment that alters the normal prostate epithelial cell differentiation program and that through this cellular process inflammation accelerates the initiation of prostate cancer with a basal cell origin.
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