ArticleMaterials today. Bio2025
3D printing-biomimetic local stiff niche enhances glycolysis to boost PDAC cell stem-like phenotype via N6-methyladenosine-suppressed YAP1 mRNA decay.
Article in Materials today. Bio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Biofabrication and artificial intelligence strategies for investigating solid- and fluid-pressure mechanobiology in pancreatic ductal adenocarcinoma.Cancer metastasis reviews · 2026Review
- Copper homeostasis and cuproptosis: molecular mechanisms and therapeutic opportunities.Molecular biomedicine · 2026Review
- The RNA methylation modification as an immunometabolic regulatory hub in pancreatic cancer: from mechanistic insights to clinical translation perspectives.Molecular cancer · 2026Review
- Interaction between m6A and YAP1 mechanotransduction pathways is essential for mechanical memory and matrix remodeling in pancreatic cancer.International journal of biological sciences · 2026Article
- Cu-doped dendritic biodegradable nanoplatforms for augmenting cuproptosis and tumor-starvation therapy through mitochondrial metabolic cascade modulation.Materials today. Bio · 2025Article
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8 authors.
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Abstract
Cancer stem cells (CSCs), the primary source of therapy resistance in pancreatic ductal adenocarcinoma (PDAC), exist in a dynamic equilibrium through tumor microenvironment (TME)-driven plasticity. However, the stiffness heterogeneity of TME within PDAC functions on tumor cell stem-like phenotypes remains unclear. Bioinformatics, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, of CSCs identified from spatial transcriptomic and single-cell datasets of PDAC lesions exhibited activated mechanical and glycolytic pathways. Detected by the nano-indenter, PDAC tissue exhibited significant stiffness heterogeneity (200-6000 Pa). Further, biomimetic local stiffness niches were engineered using the digital light-processing (DLP) 3D-printing technology and the desmoplastic bioink (gelatin methacrylate & hyaluronic acid methacrylate, GelMA&HAMA) encapsulating PDAC cells, which permits modulation of mechanical properties without altering the biochemical ligand density. Stemness markers (NANOG, OCT4), glycolysis genes (HK2, LDHA), YAP1, and N6-methyladenosine (m6A) regulators (METTL14, IGF2BP3) were evaluated via qRT-PCR and immunofluorescence. Functional assays of glycolysis and stem-like phenotype were also conducted. Dot blot, RNA stability assay, western blot, and RIP assay were exploited to clarify the level and the function of m6A modification. The local stiff niche enhanced the stem-like phenotype of PDAC cells via YAP1-boosted glycolysis. Mechanistically, local stiff niche elevated the YAP1 level via m6A (METTL14/IGF2BP3)-stabilized YAP1 mRNA, linking mechanical inputs to glycolytic-stem-like phenotype adaptations. Collectively, the local stiff niches may drive the emergence of CSCs through epigenetic and metabolic reprogramming in PDAC mechanobiology. This provides new insights for developing more precise therapeutic strategies targeting PDAC mechanical heterogeneity.
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