ArticleCell reports2022
Impad1 and Syt11 work in an epistatic pathway that regulates EMT-mediated vesicular trafficking to drive lung cancer invasion and metastasis.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- VHL-Mediated SYT11 Degradation Suppresses Gastric Cancer Cell Growth and Invasion Through Downregulation of SPINK1.Journal of cellular and molecular medicine · 2025Article
- Constructing a Novel Amino Acid Metabolism Signature: A New Perspective on Pheochromocytoma Diagnosis, Immune Landscape, and Immunotherapy.Biochemical genetics · 2025Article
- To reveal biomarkers related to macrophage and lactic acid metabolism in renal fibrosis and explore their mechanisms.Frontiers in immunology · 2025Article
- Toxicity of microplastic fibers containing azobenzene disperse dyes to human lung epithelial cells cultured at an air-liquid interface.Journal of hazardous materials · 2024Article
- Role of SYT11 in human pan-cancer using comprehensive approaches.European journal of medical research · 2024Article
- Synaptotagmin-11 facilitates assembly of a presynaptic signaling complex in post-Golgi cargo vesicles.EMBO reports · 2024Article
- Article
- Characterizing the secretome of EGFR mutant lung adenocarcinoma.Frontiers in oncology · 2023Article
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Authors and funding
15 authors at 2 institutions in 1 country.
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Abstract
Lung cancer is a highly aggressive and metastatic disease responsible for approximately 25% of all cancer-related deaths in the United States. Using high-throughput in vitro and in vivo screens, we have previously established Impad1 as a driver of lung cancer invasion and metastasis. Here we elucidate that Impad1 is a direct target of the epithelial microRNAs (miRNAs) miR-200 and miR∼96 and is de-repressed during epithelial-to-mesenchymal transition (EMT); thus, we establish a mode of regulation of the protein. Impad1 modulates Golgi apparatus morphology and vesicular trafficking through its interaction with a trafficking protein, Syt11. These changes in Golgi apparatus dynamics alter the extracellular matrix and the tumor microenvironment (TME) to promote invasion and metastasis. Inhibiting Impad1 or Syt11 disrupts the cancer cell secretome, regulates the TME, and reverses the invasive or metastatic phenotype. This work identifies Impad1 as a regulator of EMT and secretome-mediated changes during lung cancer progression.
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