ArticleNature communications2023
NLRP6 potentiates PI3K/AKT signalling by promoting autophagic degradation of p85α to drive tumorigenesis.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Propofol Inhibits Neutrophil Extracellular Traps Formation and Alleviates Sepsis-Induced Acute Lung Injury.Inflammation · 2026Article
- CD147 promotes NSCLC metastasis by inducing secretory autophagy-dependent exosome secretion via TRIM56-mediated ubiquitination and degradation of GCN2.Cell death and differentiation · 2026Article
- Piezo1/PI3K-induced autophagy dysregulation in PDLSCs under mechanical stress during root resorption.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Outer membrane vesicles fromFrontiers in microbiology · 2026Article
- Ubiquitin-Proteasome System-Related Prognostic Model and Immune Landscape in Glioblastoma.International journal of genomics · 2026Article
- NLRPs and tumor: research progress from molecular mechanisms to clinical applications.Oncogene · 2026Review
- Inflammasomes and pyroptosis in cancer: mechanisms and therapeutic advances.Journal of hematology & oncology · 2025Review
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- Targeting Intratumoral Copper Inhibits Tumor Progression via p62-Mediated EZH2 Degradation and Potentiates Anti-PD-1 Immunotherapy in Oral Squamous Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Advances on the therapeutic potential of cell receptor activation in glioblastoma.Molecular biology reports · 2025Review
- CGR11 promotes hepatocellular carcinoma progression by regulating autophagy through the PI3K/AKT pathway.Frontiers in cell and developmental biology · 2025Article
- TRIM32 promotes neuronal ferroptosis by enhancing K63-linked ubiquitination and subsequent p62-selective autophagic degradation of GPX4.International journal of biological sciences · 2025Article
- The role of pyroptosis in cancer: key components and therapeutic potential.Cell communication and signaling : CCS · 2024Review
- [Nlrp6 overexpression inhibits lipid synthesis to suppress proliferation of hepatocellular carcinoma cells by regulating the AMPK-Srebp1c axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Interaction of ncRNAs and the PI3K/AKT/mTOR pathway: Implications for osteosarcoma.Open life sciences · 2024Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The PI3K/AKT pathway plays an essential role in tumour development. NOD-like receptors (NLRs) regulate innate immunity and are implicated in cancer, but whether they are involved in PI3K/AKT pathway regulation is poorly understood. Here, we report that NLRP6 potentiates the PI3K/AKT pathway by binding and destabilizing p85α, the regulatory subunit of PI3K. Mechanistically, NLRP6 recruits the E3 ligase RBX1 to p85α and ubiquitinates lysine 256 on p85α, which is recognized by the autophagy cargo receptor OPTN, causing selective autophagic degradation of p85α and subsequent activation of the PI3K/AKT pathway by reducing PTEN stability. We further show that loss of NLRP6 suppresses cell proliferation, colony formation, cell migration, and tumour growth in glioblastoma cells in vitro and in vivo. Disruption of the NLRP6/p85α interaction using the Pep9 peptide inhibits the PI3K/AKT pathway and generates potent antitumour effects. Collectively, our results suggest that NLRP6 promotes p85α degradation via selective autophagy to drive tumorigenesis, and the interaction between NLRP6 and p85α can be a promising therapeutic target for tumour treatment.
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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.