ArticleMolecular biology of the cell2023
Differential modulation of cellular phenotype and drug sensitivity by extracellular matrix proteins in primary and metastatic pancreatic cancer cells.
Article in Molecular biology of the cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 6 citations in OpenAlex.
- Identification of Pancreatic Ductal Adenocarcinoma Extracellular Matrix Signatures from In-Depth Proteomic Profiling that Correlate with Lymphocyte Infiltration.Cancer research communications · 2026Article
- Impact of culture dimensionality and matrix composition on morphology, phenotype and drug response in pancreatic cancer models.Scientific reports · 2026Article
- Colloid-patterned surfaces distinguish malignant mechanophenotypes.Materials today. Bio · 2026Article
- Extracellular pH and NHE1 Regulate Ductal Branching Morphogenesis in Organotypic Cultures of Human Pancreatic Duct Epithelial Cells.Journal of cellular physiology · 2026Article
- Rotational migration in human pancreatic ductal organoids depends on actin and myosin activity.Communications biology · 2025Article
- Rotational migration in human pancreatic ductal organoids depends on actin and myosin activity.ArXiv · 2025Article
- Mapping Tumor-Stroma-ECM Interactions in Spatially Advanced 3D Models of Pancreatic Cancer.ACS applied materials & interfaces · 2025Article
- B3GNT5 is a novel marker correlated with malignant phenotype and poor outcome in pancreatic cancer.iScience · 2024Article
- Harnessing Plant Flavonoids to Fight Pancreatic Cancer.Current nutrition reports · 2024Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is reported to be the third highest cause of cancer-related deaths in the United States. PDAC is known for its high proportion of stroma, which accounts for 90% of the tumor mass. The stroma is made up of extracellular matrix (ECM) and nonmalignant cells such as inflammatory cells, cancer-associated fibroblasts, and lymphatic and blood vessels. Here, we decoupled the effects of the ECM on PDAC cell lines by culturing cells on surfaces coated with different ECM proteins. Our data show that the primary tumor-derived cell lines have different morphology depending on the ECM proteins on which they are cultured, while metastatic lesion-derived PDAC lines' morphology does not change with respect to the different ECM proteins. Similarly, ECM proteins modulate the proliferation rate and the gemcitabine sensitivity of the primary tumor PDAC cell lines, but not the metastatic PDAC lines. Lastly, transcriptomics analysis of the primary tumor PDAC cells cultured on different ECM proteins reveals the regulation of various pathways, such as cell cycle, cell-adhesion molecules, and focal adhesion, including the regulation of several integrin genes that are essential for ECM recognition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.