ArticlePLoS genetics2018
TGFβ signaling limits lineage plasticity in prostate cancer.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 14 citations in OpenAlex.
- Epigenetic reprogramming of lineage switching in cancer.FEBS letters · 2026Review
- A forward genetic screen identifies Sirtuin1 as a driver of neuroendocrine prostate cancer.The Journal of experimental medicine · 2026Article
- Prognostic and immunological implications of heterogeneous cell death patterns in prostate cancer.Cancer cell international · 2024Article
- The molecular determinants of phenotypic plasticity in homeostasis and neoplasia.Cancer heterogeneity and plasticity · 2024Article
- Impact of cell plasticity on prostate tumor heterogeneity and therapeutic response.American journal of clinical and experimental urology · 2024Review
- Treatment-induced stemness and lineage plasticity in driving prostate cancer therapy resistance.Cancer heterogeneity and plasticity · 2024Article
- Animal models of bone metastatic prostate cancer.Investigative and clinical urology · 2023Review
- Biology and impact of lineage plasticity in ALK-positive NSCLC: a narrative review.Translational lung cancer research · 2023Review
- Prostate cancer epidemiology and prognostic factors in the United States.Frontiers in oncology · 2023Article
- Computer classification and construction of a novel prognostic signature based on moonlighting genes in prostate cancer.Frontiers in oncology · 2022Article
- A NJournal of oncology · 2022Article
- Immunohistochemical and genetic characteristics of HPV-associated endocervical carcinoma with an invasive stratified mucin-producing carcinoma (ISMC) component.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Article
- Lineage plasticity in cancer: a shared pathway of therapeutic resistance.Nature reviews. Clinical oncology · 2020Review
- TGIF transcription factors repress acetyl CoA metabolic gene expression and promote intestinal tumor growth.Genes & development · 2019Article
- From genomics to functions: preclinical mouse models for understanding oncogenic pathways in prostate cancer.American journal of cancer research · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Although treatment options for localized prostate cancer (CaP) are initially effective, the five-year survival for metastatic CaP is below 30%. Mutation or deletion of the PTEN tumor suppressor is a frequent event in metastatic CaP, and inactivation of the transforming growth factor (TGF) ß signaling pathway is associated with more advanced disease. We previously demonstrated that mouse models of CaP based on inactivation of Pten and the TGFß type II receptor (Tgfbr2) rapidly become invasive and metastatic. Here we show that mouse prostate tumors lacking Pten and Tgfbr2 have higher expression of stem cell markers and genes indicative of basal epithelial cells, and that basal cell proliferation is increased compared to Pten mutants. To better model the primarily luminal phenotype of human CaP we mutated Pten and Tgfbr2 specifically in luminal cells, and found that these tumors also progress to invasive and metastatic cancer. Accompanying the transition to invasive cancer we observed de-differentiation of luminal tumor cells to an intermediate cell type with both basal and luminal markers, as well as differentiation to basal cells. Proliferation rates in these de-differentiated cells were lower than in either basal or luminal cells. However, de-differentiated cells account for the majority of cells in micro-metastases consistent with a preferential contribution to metastasis. We suggest that active TGFß signaling limits lineage plasticity in prostate luminal cells, and that de-differentiation of luminal tumor cells can drive progression to metastatic disease.
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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 OpenQuestion graph.