ArticleAmerican journal of cancer research2025
FTO-mediated m6A modification of QPCT promotes tumorigenesis in lung adenocarcinoma by inducing macrophage chemotaxis and M2 polarization.
Article in American journal of cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Integrative multi-omics, machine learning, and experimental validation reveal that TPM1 suppresses M2 macrophage polarization and enhances chemosensitivity in acute myeloid leukemia.Cell biology and toxicology · 2026Article
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- Reader-dependent functional duality of FTO: a context-switching node at the intersection of immune evasion and therapeutic resistance.Frontiers in immunology · 2026Review
- m6A RNA modification in tumor-associated macrophages: emerging roles in cancer immunity.Frontiers in immunology · 2025Review
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Authors and funding
9 authors.
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Abstract
Lung adenocarcinoma (LUAD), the most common histologic subtype of lung cancer, is characterized by malignant and high infiltrating. Glutaminyl-peptide cyclotransferase (QPCT) promotes cancer progression by modifying the N-terminus of chemokine C-C motif ligand 2 (CCL2) to a pyroglutamate residue and stabilizing the protein. The role of QPCT in LUAD is still unknown. QPCT mRNA and protein expression were up-regulated in clinical LUAD specimens. By generating stable HCC44 cells with QPCT overexpression and stable A549 cells with QPCT knockdown, we found that QPCT knockdown notably inhibited LUAD cell proliferation. Additionally, QPCT deletion reduced the CCL2 contents in LUAD cell supernatants and inhibited phorbol 12-myristate 13-acetate-induced THP-1 macrophage chemotaxis toward tumor cells or tumor cell conditioned medium. The CD68
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