ArticleFrontiers in cell and developmental biology2026
CNOT11 depletion is associated with autophagy-related responses and IL-6-JAK-STAT signaling in cancer cells.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: The CCR4-NOT complex is a central regulator of deadenylation-mediated mRNA decay, yet the role of its vertebrate-specific subunit CNOT11 remains unclear. Methods: We investigated the role of CNOT11 in cellular stress responses using siRNA-mediated knockdown, immunoblotting, immunoprecipitation, transcriptomic analysis, quantitative RT-PCR, ELISA, cycloheximide chase assays, actinomycin D treatment, and poly(A) tail analysis. Results: CNOT11 depletion did not markedly alter the expression of other CCR4-NOT subunits but reduced the association of CNOT10 with the complex. CNOT11 knockdown was associated with LC3-II accumulation, transcriptional upregulation of autophagy-related genes, and changes in AMPK/ULK1 signaling. Increased IL-6 expression and secretion and enhanced STAT1 and STAT3 phosphorylation were also observed. IL-6 knockdown or STAT3 inhibition partially attenuated LC3-II accumulation. Increased IL-6 expression was associated with elevated transcription, without detectable changes in mRNA stability or poly(A) tail length. Discussion: These findings suggest that CNOT11 depletion is associated with LC3-II accumulation and other autophagy-related responses, with IL-6-JAK-STAT signaling contributing partially to this phenotype. Definitive assessment of autophagic flux and the causal positioning of IL-6 signaling will require further studies using gold-standard flux assays and IL-6 rescue or neutralization approaches.
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