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        <datestamp>2026-10-05T10:46:20Z</datestamp>
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          <dc:title>Supplementary file 1_Proteomic analysis of bioprinted pancreatic tumor models under different nutrient conditions.docx</dc:title>
          <dc:creator>Busra Buyuk (25311486)</dc:creator>
          <dc:creator>Ming Li (91180)</dc:creator>
          <dc:creator>Xueer Song (25311489)</dc:creator>
          <dc:creator>Kaiming Ye (296422)</dc:creator>
          <dc:subject>Biotechnology</dc:subject>
          <dc:subject>3D bioprinting</dc:subject>
          <dc:subject>cancer-associated fibroblasts</dc:subject>
          <dc:subject>metabolic adaptation</dc:subject>
          <dc:subject>nutrient stress</dc:subject>
          <dc:subject>pancreatic ductal adenocarcinoma (PDAC)</dc:subject>
          <dc:subject>proteomics</dc:subject>
          <dc:subject>tumor microenvironment</dc:subject>
          <dc:description>Background&lt;p&gt;Pancreatic ductal adenocarcinoma (PDAC) is characterized by a dense stromal microenvironment that restricts nutrient availability and contributes to tumor adaptation. Cancer-associated fibroblasts (CAFs), extracellular matrix components, and tumor cells participate in reciprocal interactions that influence the metabolic state of PDAC tumors.&lt;/p&gt;Objective&lt;p&gt;This study investigated nutrient-associated proteomic changes in three-dimensional (3D) bioprinted PDAC–CAF tumor constructs and examined alterations in metabolic and cell-junction-related pathways under nutrient-avid and nutrient-deprived conditions.&lt;/p&gt;Methods&lt;p&gt;Three-dimensional bioprinted pancreatic tumor constructs composed primarily of PANC1 cells and cancer-associated fibroblasts (CAFs) were cultured under nutrient-avid (N) and nutrient-deprived (N−) conditions. Constructs were monitored at Days 0, 6, and 12, and Day 6 was selected for comparative proteomic analysis as an intermediate stage at which nutrient-associated structural divergence was evident while both tumor and stromal compartments remained detectable. Label-free high-resolution LC–MS/MS proteomic profiling was followed by KEGG pathway enrichment and complementary bioinformatic analyses. Selected junction-associated findings were further examined by quantitative real-time PCR.&lt;/p&gt;Results&lt;p&gt;Distinct nutrient-associated proteomic signatures were observed in the bioprinted tumor constructs. Nutrient-avid conditions were associated with enrichment of pathways including pantothenate and CoA biosynthesis, β-alanine metabolism, and arginine and proline metabolism. Nutrient-deprived conditions showed enrichment of pathways related to unsaturated fatty-acid biosynthesis, fatty-acid elongation, riboflavin metabolism, folate-associated metabolism, and terpenoid backbone biosynthesis. Nutrient-associated differences were also observed among proteins assigned to gap-junction, adherens-junction, focal-adhesion, tight-junction, and central-carbon-metabolism pathways. Selected junction-associated proteomic observations were supported at the transcript level by qPCR, although concordance between mRNA and protein abundance varied among targets.&lt;/p&gt;Conclusion&lt;p&gt;Nutrient availability was associated with distinct metabolic and junction-related proteomic signatures in 3D bioprinted PDAC–CAF constructs. These findings provide hypothesis-generating evidence of nutrient-dependent molecular remodeling within a multicellular PDAC model. Functional perturbation studies will be required to determine the causal and therapeutic relevance of the candidate proteins and pathways identified here.&lt;/p&gt;</dc:description>
          <dc:date>2026-10-05T10:46:20Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fbioe.2026.1921652.s001</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/Supplementary_file_1_Proteomic_analysis_of_bioprinted_pancreatic_tumor_models_under_different_nutrient_conditions_docx/34069239</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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