ArticleInternational journal of obesity (2005)2018
Adipocytes sustain pancreatic cancer progression through a non-canonical WNT paracrine network inducing ROR2 nuclear shuttling.
Article in International journal of obesity (2005), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 40 citations in OpenAlex.
- Profilin and Non-Canonical Wnt Signaling: Coordinating Cytoskeletal Dynamics from Development to Disease.Journal of developmental biology · 2025Review
- Therapeutic advances in the targeting of ROR1 in hematological cancers.Cell death discovery · 2024Review
- Article
- Navigating Tumour Microenvironment and Wnt Signalling Crosstalk: Implications for Advanced Cancer Therapeutics.Cancers · 2023Review
- Article
- Emerging Role of Epigenetic Alterations as Biomarkers and Novel Targets for Treatments in Pancreatic Ductal Adenocarcinoma.Cancers · 2022Review
- The Ror-Family Receptors in Development, Tissue Regeneration and Age-Related Disease.Frontiers in cell and developmental biology · 2022Review
- Pancreatic Progenitor Commitment Is Marked by an Increase in Ink4a/Arf Expression.Biomolecules · 2021Article
- Pancreatic Cancer and Therapy: Role and Regulation of Cancer Stem Cells.International journal of molecular sciences · 2021Review
- Review
- Epigenetic Regulation of the Wnt/β-Catenin Signaling Pathway in Cancer.Frontiers in genetics · 2021Review
- Classifying the Linkage between Adipose Tissue Inflammation and Tumor Growth through Cancer-Associated Adipocytes.Molecules and cells · 2020Review
- Article
- The Role of Dysfunctional Adipose Tissue in Pancreatic Cancer: A Molecular Perspective.Cancers · 2020Review
- Article
- Organoid-Transplant Model Systems to Study the Effects of Obesity on the Pancreatic CarcinogenesisFrontiers in cell and developmental biology · 2020Article
- Cancer‑associated adipocytes exhibit distinct phenotypes and facilitate tumor progression in pancreatic cancer.Oncology reports · 2019Article
- Obesity-Linked Cancers: Current Knowledge, Challenges and Limitations in Mechanistic Studies and Rodent Models.Cancers · 2018Review
- Pancreatic Cancer and Obesity: Molecular Mechanisms of Cell Transformation and Chemoresistance.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSolid epidemiological evidences connect obesity with incidence, stage and survival in pancreatic cancer. However, the underlying mechanistic basis linking adipocytes to pancreatic cancer progression remain largely elusive. We hypothesized that factors secreted by adipocytes could be responsible for epithelial-to-mesenchymal transition (EMT) induction and, in turn, a more aggressive phenotype in models of pancreatic preneoplastic lesions.
methodsWe studied the role of factors secreted by two adipogenic model systems from primary human bone marrow stromal cells (hBMSCs) in an in vitro experimental cell transformation model system of human pancreatic ductal epithelial (HPDE) cell stably expressing activated KRAS (HPDE/KRAS),Results:We measured a significant induction of EMT and aggressiveness in HPDE and HPDE/KRAS cell lines when cultured with medium conditioned by fully differentiated adipocytes (ADIPO
conclusionsWe demonstrated that adipocytes could induce EMT and aggressiveness in models of pancreatic preneoplastic lesions by orchestrating a complex paracrine signaling of soluble modulators of the non-canonical WNT signaling pathway that determine, in turn, the activation and nuclear translocation of ROR2. This signaling pathway could represent a novel target for pancreatic cancer chemoprevention. Most importantly, these factors could serve as novel biomarkers to select a risk population among obese subjects for screening and, thus, early diagnosis of pancreatic cancer.
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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.