ArticleMolecular and cellular biology2013
Atypical protein kinase C phosphorylates Par6 and facilitates transforming growth factor β-induced epithelial-to-mesenchymal transition.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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
48 citing papers in PubMed, 79 citations in OpenAlex.
- Par6/SOX2 interact to modulate stemness maintenance in glioma by regulating the EGFR/PI3K/AKT signaling cascade.Oncogene · 2025Article
- Cell polarity proteins promote macropinocytosis in response to metabolic stress.Nature communications · 2024Article
- Atypical Protein Kinase C Promotes its own Asymmetric Localisation by Phosphorylating Cdc42 in thebioRxiv : the preprint server for biology · 2024Article
- Expanding the Chemical Space of Transforming Growth Factor-β (TGFβ) Receptor Type II Degraders with 3,4-Disubstituted Indole Derivatives.ACS pharmacology & translational science · 2024Article
- 14-3-3 and Smad2/3 are crucial mediators of atypical-PKCs: Implications for neuroblastoma progression.Frontiers in oncology · 2023Article
- TGF-beta signal transduction: biology, function and therapy for diseases.Molecular biomedicine · 2022Review
- Article
- Apical-basal polarity and the control of epithelial form and function.Nature reviews. Molecular cell biology · 2022Review
- Targeting Protein Kinase C for Cancer Therapy.Cancers · 2022Review
- Asymmetric Cell Division and Tumor Heterogeneity.Frontiers in cell and developmental biology · 2022Review
- Article
- Atypical PKCs activate Vimentin to facilitate prostate cancer cell motility and invasion.Cell adhesion & migration · 2021Article
- Orchestration of tissue-scale mechanics and fate decisions by polarity signalling.The EMBO journal · 2021Review
- theLiTE™: A Screening Platform to Identify Compounds that Reinforce Tight Junctions.Frontiers in pharmacology · 2021Review
- The synthetic oleanane triterpenoid CDDO-Me binds and inhibits pyruvate kinase M2.Pharmacological reports : PR · 2020Article
- Transcription co-activator P300 activates Elk1-aPKC-ι signaling mediated epithelial-to-mesenchymal transition and malignancy in hepatocellular carcinoma.Oncogenesis · 2020Article
- Review
- Effects of Atypical Protein Kinase C Inhibitor (DNDA) on Lung Cancer Proliferation and Migration by PKC-ι/FAK Ubiquitination Through the Cbl-b Pathway.OncoTargets and therapy · 2020Article
- Attenuation of amyloid-β generation by atypical protein kinase C-mediated phosphorylation of engulfment adaptor PTB domain containing 1 threonine 35.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Apical-basal polarity inhibits epithelial-mesenchymal transition and tumour metastasis by PAR-complex-mediated SNAI1 degradation.Nature cell biology · 2019Article
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3 authors at 1 institution in 1 country.
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Abstract
Epithelial-to-mesenchymal transition (EMT) is controlled by cellular signaling pathways that trigger the loss of cell-cell adhesion and lead to the restructuring of the cell cytoskeleton. Transforming growth factor β (TGF-β) has been shown to regulate cell plasticity through the phosphorylation of Par6 on a conserved serine residue (S345) by the type II TGF-β receptor. We show here that atypical protein kinase C (aPKC) is an essential component to this signaling pathway in non-small-cell lung cancer (NSCLC) cells. We show that the aPKC, PKCι, interacts with TGF-β receptors through Par6 and that these proteins localize to the leading edge of migrating cells. Furthermore, Par6 phosphorylation on serine 345 by TGF-β receptors is enhanced in the presence of aPKC. aPKC kinase activity, as well as an association with Par6, were found to be important for Par6 phosphorylation. In effect, small interfering RNA-targeting aPKC reduces TGF-β-induced RhoA and E-cadherin loss, cell morphology changes, stress fiber production, and the migration of NSCLC cells. Interestingly, reintroduction of a phosphomimetic Par6 (Par6-S345E) into aPKC-silenced cells rescues both RhoA and E-cadherin loss with TGF-β stimulation. In conclusion, our results suggest that aPKCs cooperate with TGF-β receptors to regulate phospho-Par6-dependent EMT and cell migration.
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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.