ArticleOncogene2017
PKCι regulates nuclear YAP1 localization and ovarian cancer tumorigenesis.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
- Protein kinase Cι dictates tumor trajectory, cell plasticity, and immune surveillance in lung adenocarcinoma.Cell reports · 2025Article
- Auranofin Synergizes with Cisplatin in Reducing Tumor Burden of NOTCH-Dependent Ovarian Cancer.Cancer research communications · 2025Article
- The multifaceted role of YAP in the tumor microenvironment and its therapeutic implications in cancer.Experimental & molecular medicine · 2025Review
- Prkci promotes colorectal cancer metastasis by phosphorylating and stabilizing Tgfbr1 to activate TGF-β signaling.Cell communication and signaling : CCS · 2025Article
- Association of low angiomotin-p130 and high YAP1 nuclear expression with adverse prognosis in epithelial ovarian cancer.Histology and histopathology · 2025Article
- Protein kinase C iota promotes glycolysis via PI3K/AKT/mTOR signalling in high grade serous ovarian cancer.Molecular biology reports · 2024Article
- Role of angiomotin family members in human diseases (Review).Experimental and therapeutic medicine · 2024Review
- Determining the minimal amount of DMSO necessary to stabilize the Angiomotin lipid binding domain.Indiana University journal of undergraduate research · 2024Article
- Amplified therapeutic targets in high-grade serous ovarian carcinoma - a review of the literature with quantitative appraisal.Cancer gene therapy · 2023Review
- Review
- CircAMOTL1 RNA and AMOTL1 Protein: Complex Functions ofInternational journal of molecular sciences · 2023Review
- Protein kinase Cι mediates immunosuppression in lung adenocarcinoma.Science translational medicine · 2022Article
- Protein Kinase C (PKC) Isozymes as Diagnostic and Prognostic Biomarkers and Therapeutic Targets for Cancer.Cancers · 2022Review
- Inhibition of PKC-δ reduce rhabdomyolysis-induced acute kidney injury.Journal of cellular and molecular medicine · 2022Article
- YAP/Hippo Pathway and Cancer Immunity: It Takes Two to Tango.Biomedicines · 2021Review
- A novel somatic mutation in GNB2 provides new insights to the pathogenesis of Sturge-Weber syndrome.Human molecular genetics · 2021Article
- Review
- Angiomotin-p130 inhibits vasculogenic mimicry formation of small cell lung cancer independently of Smad2/3 signal pathway.Journal of bioenergetics and biomembranes · 2021Article
- Long non‑coding RNAInternational journal of molecular medicine · 2021Article
- CLIC1 knockout inhibits invasion and migration of gastric cancer by upregulating AMOT-p130 expression.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Atypical protein kinase Cι (PKCι) is an oncogene in lung and ovarian cancer. The PKCι gene PRKCI is targeted for frequent tumor-specific copy number gain (CNG) in both lung squamous cell carcinoma (LSCC) and ovarian serous carcinoma (OSC). We recently demonstrated that in LSCC cells PRKCI CNG functions to drive transformed growth and tumorigenicity by activating PKCι-dependent cell autonomous Hedgehog (Hh) signaling. Here, we assessed whether OSC cells harboring PRKCI CNG exhibit similar PKCι-dependent Hh signaling. Surprisingly, we find that whereas PKCι is required for the transformed growth of OSC cells harboring PRKCI CNG, these cells do not exhibit PKCι-dependent Hh signaling or Hh-dependent proliferation. Rather, transformed growth of OSC cells is regulated by PKCι-dependent nuclear localization of the oncogenic transcription factor, YAP1. Lentiviral shRNA-mediated knockdown (KD) of PKCι leads to decreased nuclear YAP1 and increased YAP1 binding to angiomotin (AMOT), which sequesters YAP1 in the cytoplasm. Biochemical analysis reveals that PKCι directly phosphorylates AMOT at a unique site, Thr750, whose phosphorylation inhibits YAP1 binding. Pharmacologic inhibition of PKCι decreases YAP1 nuclear localization and blocks OSC tumor growth in vitro and in vivo. Immunohistochemical analysis reveals a strong positive correlation between tumor PKCι expression and nuclear YAP1 in primary OSC tumor samples, indicating the clinical relevance of PKCι-YAP1 signaling. Our results uncover a novel PKCι-AMOT-YAP1 signaling axis that promotes OSC tumor growth, and provide a rationale for therapeutic targeting of this pathway for treatment of OSC.
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