ArticleJournal of molecular cell biology2018
Tgfbr2 inactivation facilitates cellular plasticity and development of Pten-null prostate cancer.
Article in Journal of molecular cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- ATXN3 promotes prostate cancer progression by stabilizing YAP.Cell communication and signaling : CCS · 2023Article
- Imbalance of TGF-β1/BMP-7 pathways induced by M2-polarized macrophages promotes hepatocellular carcinoma aggressiveness.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Regulation of stem/progenitor cell maintenance by BMP5 in prostate homeostasis and cancer initiation.eLife · 2020Article
- Opposing roles and potential antagonistic mechanism between TGF-β and BMP pathways: Implications for cancer progression.EBioMedicine · 2019Review
- TMEFF1 overexpression and its mechanism for tumor promotion in ovarian cancer.Cancer management and research · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Mutations in tumors can create a state of increased cellular plasticity that promotes resistance to treatment. Thus, there is an urgent need to develop novel strategies for identifying key factors that regulate cellular plasticity in order to combat resistance to chemotherapy and radiation treatment. Here we report that prostate epithelial cell reprogramming could be exploited to identify key factors required for promoting prostate cancer tumorigenesis and cellular plasticity. Deletion of phosphatase and tensin homolog (Pten) and transforming growth factor-beta receptor type 2 (Tgfbr2) may increase prostate epithelial cell reprogramming efficiency in vitro and cause rapid tumor development and early mortality in vivo. Tgfbr2 ablation abolished TGF-β signaling but increased the bone morphogenetic protein (BMP) signaling pathway through the negative regulator Tmeff1. Furthermore, increased BMP signaling promotes expression of the tumor marker genes ID1, Oct4, Nanog, and Sox2; ID1/STAT3/NANOG expression was inversely correlated with patient survival. Thus, our findings provide information about the molecular mechanisms by which BMP signaling pathways render stemness capacity to prostate tumor cells.
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Registered trials
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