ArticleAutophagy2024
An autophagy-independent role of ULK1/ULK2 in mechanotransduction and breast cancer cell migration.
Article in Autophagy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Prenatal exposure to polystyrene nanoplastics impairs offspring fertility in mice by disrupting meiotic recombination and chromatin accessibility in oocytes.Archives of toxicology · 2026Article
- The Role of ULK3 in Cancer Progression: A Pan-Cancer Bioinformatics Analysis Integrated with Experimental Validation in Prostate Cancer.International journal of molecular sciences · 2026Article
- In silico identification of bilobetin and ginsenoside as dual CK2 and ULK2 inhibitors targeting triple-negative breast cancer.Scientific reports · 2025Article
- Genetic associations of plasma proteins and breast cancer identify potential therapeutic drug candidates.Communications biology · 2025Article
- Breast Cancer: Extracellular Matrix and Microbiome Interactions.International journal of molecular sciences · 2024Review
- ULK2 suppresses glycolysis to attenuate cisplatin resistance in ovarian cancer organoid via c-Jun phosphorylation.Science progressArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The progression of breast cancer is often accompanied by changes in extracellular matrix stiffness and cell adhesion ability, which are closely related to cellular mechanotransduction. However, the underlying regulatory mechanisms remain mysterious. Our study reveals that the macroautophagy/autophagy-inducing kinases, ULK1 and ULK2, inhibit the assembly of focal adhesions and F-actin by phosphorylating the adhesion protein PXN, to prevent breast cancer cell migration in an autophagy-independent fashion. Interestingly, ULK1/ULK2-mediated serine phosphorylation of PXN counteracts PXN phosphorylation at the adjacent tyrosine residues by PTK2 and SRC, to gatekeep cellular mechanotransduction. Our research establishes a new function of ULK1/ULK2 in governing cellular mechanotransduction that might be harnessed for treating breast cancer.
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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.