ArticleNeoplasia (New York, N.Y.)2011
Cooperation between Stat3 and Akt signaling leads to prostate tumor development in transgenic mice.
Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- SRRT promotes prostate cancer progression and serves as a prognostic biomarker through STAT3 pathway activation.Oncology reports · 2026Article
- Impact of STAT Proteins in Tumor Progress and Therapy Resistance in Advanced and Metastasized Prostate Cancer.Cancers · 2021Review
- Phosphatidylinositol 3,4,5-Trisphosphate-Dependent Rac Exchanger 2 Protein Facilitates Glioma Progression via Akt and Stat3 Signaling.Journal of molecular neuroscience : MN · 2021Article
- PI3Kγ inhibition suppresses microglia/TAM accumulation in glioblastoma microenvironment to promote exceptional temozolomide response.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Review
- 27-Hydroxycholesterol Impairs Plasma Membrane Lipid Raft Signaling as Evidenced by Inhibition of IL6-JAK-STAT3 Signaling in Prostate Cancer Cells.Molecular cancer research : MCR · 2020Article
- IL22 drives cutaneous melanoma cell proliferation, migration and invasion through activation of miR-181/STAT3/AKT axis.Journal of Cancer · 2020Article
- Evaluation of the STAT3 inhibitor GLG‑302 for the prevention of estrogen receptor‑positive and ‑negative mammary cancers.Oncology reports · 2019Article
- Protein Kinase C Epsilon Cooperates with PTEN Loss for Prostate Tumorigenesis through the CXCL13-CXCR5 Pathway.Cell reports · 2017Article
- Article
- Induction of metastatic potential by TrkB via activation of IL6/JAK2/STAT3 and PI3K/AKT signaling in breast cancer.Oncotarget · 2015Article
- A novel mechanism of skin tumor promotion involving interferon-gamma (IFNγ)/signal transducer and activator of transcription-1 (Stat1) signaling.Molecular carcinogenesis · 2015Article
- Prostate cancer stem cells: deciphering the origins and pathways involved in prostate tumorigenesis and aggression.Oncotarget · 2015Review
- A human prostatic bacterial isolate alters the prostatic microenvironment and accelerates prostate cancer progression.The Journal of pathology · 2015Article
- The ETS family member GABPα modulates androgen receptor signalling and mediates an aggressive phenotype in prostate cancer.Nucleic acids research · 2014Article
- Article
- Article
- Cancer subclonal genetic architecture as a key to personalized medicine.Neoplasia (New York, N.Y.) · 2013Article
- JNK and STAT3 signaling pathways converge on Akt-mediated phosphorylation of EZH2 in bronchial epithelial cells induced by arsenic.Cell cycle (Georgetown, Tex.) · 2013Article
- Overcoming intratumor heterogeneity of polygenic cancer drug resistance with improved biomarker integration.Neoplasia (New York, N.Y.) · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
In this report, we describe the development of a transgenic mouse in which a rat probasin promoter (ARR(2)Pb) was used to direct prostate specific expression of a constitutively active form of signal transducer and activator of transcription 3 (i.e., Stat3C). ARR(2)Pb.Stat3C mice exhibited hyperplasia and prostate intraepithelial neoplasia (PIN) lesions in both ventral and dorsolateral prostate lobes at 6 and 12 months; however, no adenocarcinomas were detected. The effect of combined loss of PTEN was examined by crossing ARR(2)Pb.Stat3C mice with PTEN(+/-) null mice. PTEN(+/-) null mice on an ICR genetic background developed only hyperplasia and PIN at 6 and 12 months, respectively. ARR(2)Pb.Stat3C x PTEN(+/-) mice exhibited a more severe prostate phenotype compared with ARR(2)Pb.Stat3C and PTEN(+/-) mice. ARR(2)Pb.Stat3C x PTEN(+/-) mice developed adenocarcinomas in the ventral prostate as early as 6 months (22% incidence) that reached an incidence of 61% by 12 months. Further evaluations indicated that phospho-Stat3, phospho-Akt, phospho-nuclear factor κB, cyclin D1, and Ki67 were upregulated in adenocarcinomas from ARR(2)Pb.Stat3C x PTEN(+/-) mice. In addition, membrane staining for β-catenin and E-cadherin was reduced. The changes in Stat3 and nuclear factor κB phosphorylation correlated most closely with tumor progression. Collectively, these data provide evidence that Stat3 and Akt signaling cooperate in prostate cancer development and progression and that ARR(2)Pb.Stat3C x PTEN(+/-) mice represent a novel mouse model of prostate cancer to study these interactions.
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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.