ArticleCells2018
Tumor⁻Stroma Cross-Talk in Human Pancreatic Ductal Adenocarcinoma: A Focus on the Effect of the Extracellular Matrix on Tumor Cell Phenotype and Invasive Potential.
Article in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 54 citations in OpenAlex.
- Molecular Imaging in Pancreatic Cancer: Current Applications and Future Perspectives.Pharmaceuticals (Basel, Switzerland) · 2026Review
- GPX8Oncogene · 2026Article
- A 3D Bioprinted Pancreatic Cancer Model Using Collagen-Gelatin Methacrylamide-Alginate Bioinks to Mimic the Desmoplastic Microenvironment.Biomacromolecules · 2025Article
- The application of organoids in treatment decision-making for digestive system cancers: progress and challenges.Molecular cancer · 2025Review
- New insights into Notch signaling as a crucial pathway of pancreatic cancer stem cell behavior by chrysin-polylactic acid-based nanocomposite.Discover oncology · 2025Review
- Multiphoton excited polymerized biomimetic models of collagen fiber morphology to study single cell and collective migration dynamics in pancreatic cancer.Acta biomaterialia · 2024Article
- Machine learning-based approach for automated classification of cell and extracellular matrix using nanomechanical properties.Materials today. Bio · 2024Article
- Dysregulation of intercellular communication in vitro and in vivo via extracellular vesicles secreted by pancreatic duct adenocarcinoma cells and generated under the influence of the AG9 elastin peptide-conditioned microenvironment.Journal of extracellular biology · 2024Article
- A multimodal imaging study to highlight elastin-derived peptide pro-tumoral effect in a pancreatic xenograft model.British journal of cancer · 2023Article
- Pancreatic Organoids: A Frontier Method for Investigating Pancreatic-Related Diseases.International journal of molecular sciences · 2023Review
- Identification and verification of CCNB1 as a potential prognostic biomarker by comprehensive analysis.Scientific reports · 2022Article
- Cancer associated fibroblast-derived CCL5 promotes hepatocellular carcinoma metastasis through activating HIF1α/ZEB1 axis.Cell death & disease · 2022Article
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- Cold Atmospheric Plasma Does Not Affect Stellate Cells Phenotype in Pancreatic Cancer Tissue in Ovo.International journal of molecular sciences · 2022Article
- The Urokinase Plasminogen Activation System in Pancreatic Cancer: Prospective Diagnostic and Therapeutic Targets.Biomolecules · 2022Review
- Pancreatic Cancer Small Extracellular Vesicles (Exosomes): A Tale of Short- and Long-Distance Communication.Cancers · 2021Review
- Implications of prognosis-associated genes in pancreatic tumor metastasis: lessons from global studies in bioinformatics.Cancer metastasis reviews · 2021Review
- Collagenase-ExpressingCancers · 2021Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The extracellular matrix (ECM) in the tumor microenvironment modulates the cancer cell phenotype, especially in pancreatic ductal adenocarcinoma (PDAC), a tumor characterized by an intense desmoplastic reaction. Because the epithelial-to-mesenchymal transition (EMT), a process that provides cancer cells with a metastatic phenotype, plays an important role in PDAC progression, the authors aimed to explore in vitro the interactions between human PDAC cells and ECM components of the PDAC microenvironment, focusing on the expression of EMT markers and matrix metalloproteinases (MMPs) that are able to digest the basement membrane during tumor invasion. EMT markers and the invasive potential of HPAF-II, HPAC, and PL45 cells grown on different ECM substrates (fibronectin, laminin, and collagen) were analyzed. While N-cadherin, αSMA, and type I collagen were not significantly affected by ECM components, the E-cadherin/β-catenin complex was highly expressed in all the experimental conditions, and E-cadherin was upregulated by collagen in PL45 cells. Cell migration was unaffected by fibronectin and delayed by laminin. In contrast, collagen significantly stimulated cell migration and the secretion of MMPs. This study's results showed that ECM components impacted cell migration and invasive potential differently. Collagen exerted a more evident effect, providing new insights into the understanding of the intricate interplay between ECM molecules and cancer cells, in order to find novel therapeutic targets for PDAC treatment.
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What OpenQuestion holds
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.