ArticleThe Journal of biological chemistry2015
Loss of the polarity protein PAR3 activates STAT3 signaling via an atypical protein kinase C (aPKC)/NF-κB/interleukin-6 (IL-6) axis in mouse mammary cells.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Review
- Inhibition of Pard3 promotes breast cancer metastasis via the USP28 mediated deubiquitination of Snail1.Heliyon · 2023Article
- Bile reflux and hypopharyngeal cancer (Review).Oncology reports · 2021Review
- Loss of polarity protein Par3, via transcription factor Snail, promotes bladder cancer metastasis.Cancer science · 2021Article
- The molecular basis of mammary gland development and epithelial differentiation.Seminars in cell & developmental biology · 2021Review
- Pepsin Promotes Activation of Epidermal Growth Factor Receptor and Downstream Oncogenic Pathways, at Slightly Acidic and Neutral pH, in Exposed Hypopharyngeal Cells.International journal of molecular sciences · 2021Article
- Interactions and Feedbacks in E-Cadherin Transcriptional Regulation.Frontiers in cell and developmental biology · 2021Article
- Diversified Application of Barcoded PLATO (PLATO-BC) Platform for Identification of Protein Interactions.Genomics, proteomics & bioinformatics · 2019Article
- Temporal characteristics of NF-κB inhibition in blocking bile-induced oncogenic molecular events in hypopharyngeal cells.Oncotarget · 2019Article
- Apical-basal polarity inhibits epithelial-mesenchymal transition and tumour metastasis by PAR-complex-mediated SNAI1 degradation.Nature cell biology · 2019Article
- Curcumin prevents the bile reflux-induced NF-κB-related mRNA oncogenic phenotype, in human hypopharyngeal cells.Journal of cellular and molecular medicine · 2018Article
- Article
- NF-κB inhibition reverses acidic bile-induced miR-21, miR-155, miR-192, miR-34a, miR-375 and miR-451a deregulations in human hypopharyngeal cells.Journal of cellular and molecular medicine · 2018Article
- A DNA nanorobot functions as a cancer therapeutic in response to a molecular trigger in vivo.Nature biotechnology · 2018Article
- Inhibition of NF-Oncotarget · 2018Article
- Mechanisms of cell competition emerging from Drosophila studies.Current opinion in cell biology · 2017Article
- Par3 integrates Tiam1 and phosphatidylinositol 3-kinase signaling to change apical membrane identity.Molecular biology of the cell · 2017Article
- Expression of Par3 polarity protein correlates with poor prognosis in ovarian cancer.BMC cancer · 2016Article
- Conditional knockout of polarity complex (atypical) PKCι reveals an anti-inflammatory function mediated by NF-κB.Molecular biology of the cell · 2016Article
- Molecular Control of Atypical Protein Kinase C: Tipping the Balance between Self-Renewal and Differentiation.Journal of molecular biology · 2016Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
PAR3 suppresses tumor growth and metastasis in vivo and cell invasion through matrix in vitro. We propose that PAR3 organizes and limits multiple signaling pathways and that inappropriate activation of these pathways occurs without PAR3. Silencing Pard3 in conjunction with oncogenic activation promotes invasion and metastasis via constitutive STAT3 activity in mouse models, but the mechanism for this is unknown. We now show that loss of PAR3 triggers increased production of interleukin-6, which induces STAT3 signaling in an autocrine manner. Activation of atypical protein kinase C ι/λ (aPKCι/λ) mediates this effect by stimulating NF-κB signaling and IL-6 expression. Our results suggest that PAR3 restrains aPKCι/λ activity and thus prevents aPKCι/λ from activating an oncogenic signaling network.
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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.