ArticleCell reports2017
The ULK3 Kinase Is Critical for Convergent Control of Cancer-Associated Fibroblast Activation by CSL and GLI.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
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- Notch signaling in the tumor microenvironment: recent advances and targeted therapeutics.Molecular cancer · 2026Review
- Unc-51 like kinase 3 induces reticulophagy by mediating the GLI1/CAMK2B signaling pathway to promote the malignant progression of prostate cancer.American journal of cancer research · 2026Article
- The Parkinson Disease-Associated Mutant DNAJC13(N855S) Leads to Its Accelerated Degradation and Negatively Affects Macroautophagy and Retromer Complex-Mediated Dynamics.Journal of cellular physiology · 2025Article
- Autophagy mediated immune response regulation and drug resistance in cancer.Molecular biology reports · 2025Review
- Morphogen-induced kinase condensates transduce Hh signal by allosterically activating Gli.Science advances · 2025Article
- BIN1 deficiency enhances ULK3-dependent autophagic flux and reduces dendritic size in mouse hippocampal neurons.Autophagy · 2025Article
- Identification of autophagy-related genes and immune cell infiltration characteristics in sepsis via bioinformatic analysis.Journal of thoracic disease · 2023Article
- Article
- The ULK3 kinase is a determinant of keratinocyte self-renewal and tumorigenesis targeting the arginine methylome.Nature communications · 2023Article
- Small Molecule Inhibitors for Unc-51-like Autophagy-Activating Kinase Targeting Autophagy in Cancer.International journal of molecular sciences · 2023Review
- Role of autophagy in cancer-associated fibroblast activation, signaling and metabolic reprograming.Frontiers in cell and developmental biology · 2023Review
- Signaling pathways in cancer-associated fibroblasts: recent advances and future perspectives.Cancer communications (London, England) · 2023Review
- ULK3-dependent activation of GLI1 promotes DNMT3A expression upon autophagy induction.Autophagy · 2022Article
- Exosomal non-coding RNAs have a significant effect on tumor metastasis.Molecular therapy. Nucleic acids · 2022Review
- Autophagy-related DjAtg1-1 plays critical role in planarian regeneration by regulating proliferation and cell death.Cell and tissue research · 2022Article
- Functional genomics atlas of synovial fibroblasts defining rheumatoid arthritis heritability.Genome biology · 2021Article
- Merkel cell carcinoma-derived exosome-shuttle miR-375 induces fibroblast polarization by inhibition of RBPJ and p53.Oncogene · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The connection between signaling pathways activating cancer-associated fibroblasts (CAFs) remains to be determined. Metabolic alterations linked to autophagy have also been implicated in CAF activation. CSL/RBPJ, a transcriptional repressor that mediates Notch signaling, suppresses the gene expression program(s), leading to stromal senescence and CAF activation. Deregulated GLI signaling can also contribute to CAF conversion. Here, we report that compromised CSL function depends on GLI activation for conversion of human dermal fibroblasts into CAFs, separately from cellular senescence. Decreased CSL upregulates the expression of the ULK3 kinase, which binds and activates GLI2. Increased ULK3 also induces autophagy, which is unlinked from GLI and CAF activation. ULK3 upregulation occurs in the CAFs of several tumor types, and ULK3 silencing suppresses the tumor-enhancing properties of these cells. Thus, ULK3 links two key signaling pathways involved in CAF conversion and is an attractive target for stroma-focused anti-cancer intervention.
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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.