ALDOA coordinates PDE3A through the β-catenin/ID3 axis to stimulate cancer metastasis and M2 polarization in lung cancer with EGFR mutations.

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  • Additional Information
    • Source:
      Publisher: Elsevier Country of Publication: United States NLM ID: 0372516 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1090-2104 (Electronic) Linking ISSN: 0006291X NLM ISO Abbreviation: Biochem Biophys Res Commun Subsets: MEDLINE
    • Publication Information:
      Publication: <2002- >: San Diego, CA : Elsevier
      Original Publication: New York, Academic Press.
    • Subject Terms:
      Lung Neoplasms*/drug therapy ; Lung Neoplasms*/genetics ; Lung Neoplasms*/pathology; Humans ; Fructose-Bisphosphate Aldolase/genetics ; beta Catenin/genetics ; beta Catenin/metabolism ; Signal Transduction/genetics ; Cyclic Nucleotide Phosphodiesterases, Type 3/genetics ; Cyclic Nucleotide Phosphodiesterases, Type 3/metabolism ; Cell Line, Tumor ; Mutation ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Neoplasm Proteins/metabolism ; Inhibitor of Differentiation Proteins/genetics
    • Abstract:
      Lung cancer has a high incidence rate and requires more effective treatment strategies and drug options for clinical patients. EGFR is a common genetic alteration event in lung cancer that affects patient survival and drug strategy. Our study discovered aberrant aldolase A (ALDOA) expression and dysfunction in lung cancer patients with EGFR mutations. In addition to investigating relevant metabolic processes like glucose uptake, lactate production, and ATPase activity, we examined multi-omics profiles (transcriptomics, proteomics, and pull-down assays). It was observed that phosphodiesterase 3A (PDE3A) enzyme and ALDOA exhibit correlation, and furthermore, they impact M2 macrophage polarization through β-catenin and downstream ID3. In addition to demonstrating the aforementioned mechanism of action, our experiments discovered that the PDE3 inhibitor trequinsin has a substantial impact on lung cancer cell lines with EGFR mutants. The trequinsin medication was found to decrease the M2 macrophage polarization status and several cancer phenotypes, in addition to transduction. These findings have potential prognostic and therapeutic applications for clinical patients with EGFR mutation and lung cancer.
      Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
      (Copyright © 2024 Elsevier Inc. All rights reserved.)
    • Contributed Indexing:
      Keywords: ALDOA; EGFR mutant; Lung cancer; PDE3; Trequinsin
    • Accession Number:
      EC 4.1.2.13 (Fructose-Bisphosphate Aldolase)
      0 (beta Catenin)
      EC 3.1.4.17 (Cyclic Nucleotide Phosphodiesterases, Type 3)
      EC 2.7.10.1 (ErbB Receptors)
      147785-34-0 (ID3 protein, human)
      0 (Neoplasm Proteins)
      0 (Inhibitor of Differentiation Proteins)
      EC 3.1.4.17 (PDE3A protein, human)
      EC 2.7.10.1 (EGFR protein, human)
      EC 4.1.2.13 (ALDOA protein, human)
    • Publication Date:
      Date Created: 20240120 Date Completed: 20240202 Latest Revision: 20240909
    • Publication Date:
      20240910
    • Accession Number:
      10.1016/j.bbrc.2024.149489
    • Accession Number:
      38244313