ArticleCarcinogenesis2014
The neuroendocrine phenotype of gastric myofibroblasts and its loss with cancer progression.
Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Depression accelerates gastric cancer invasion and metastasis by inducing a neuroendocrine phenotype via the catecholamine/βCancer communications (London, England) · 2021Article
- Integrated omics profiling reveals novel patterns of epigenetic programming in cancer-associated myofibroblasts.Carcinogenesis · 2019Article
- Integrative Omic Profiling Reveals Unique Hypoxia Induced Signatures in Gastric Cancer Associated Myofibroblasts.Cancers · 2019Article
- Chemerin acts via CMKLR1 and GPR1 to stimulate migration and invasion of gastric cancer cells: putative role of decreased TIMP-1 and TIMP-2.Oncotarget · 2019Article
- Stable Isotope Dynamic Labeling of Secretomes (SIDLS) Identifies Authentic Secretory Proteins Released by Cancer and Stromal Cells.Molecular & cellular proteomics : MCP · 2018Article
- Matrix metalloproteinase (MMP)-7 in Barrett's esophagus and esophageal adenocarcinoma: expression, metabolism, and functional significance.Physiological reports · 2018Article
- Cell cycle dependent expression of the CCK2 receptor by gastrointestinal myofibroblasts: putative role in determining cell migration.Physiological reports · 2017Article
- Dies1/VISTA expression loss is a recurrent event in gastric cancer due to epigenetic regulation.Scientific reports · 2016Article
- The role of chemerin and ChemR23 in stimulating the invasion of squamous oesophageal cancer cells.British journal of cancer · 2016Article
- Distinct miRNA profiles in normal and gastric cancer myofibroblasts and significance in Wnt signaling.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Cancer-associated fibroblasts promote angiogenesis in gastric cancer through galectin-1 expression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
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Authors and funding
19 authors at 3 institutions in 3 countries.
Funding
Abstract
Stromal cells influence cancer progression. Myofibroblasts are an important stromal cell type, which influence the tumour microenvironment by release of extracellular matrix (ECM) proteins, proteases, cytokines and chemokines. The mechanisms of secretion are poorly understood. Here, we describe the secretion of marker proteins in gastric cancer and control myofibroblasts in response to insulin-like growth factor (IGF) stimulation and, using functional genomic approaches, we identify proteins influencing the secretory response. IGF rapidly increased myofibroblast secretion of an ECM protein, TGFβig-h3. The secretory response was not blocked by inhibition of protein synthesis and was partially mediated by increased intracellular calcium (Ca(2+)). The capacity for evoked secretion was associated with the presence of dense-core secretory vesicles and was lost in cells from patients with advanced gastric cancer. In cells responding to IGF-II, the expression of neuroendocrine marker proteins, including secretogranin-II and proenkephalin, was identified by gene array and LC-MS/MS respectively, and verified experimentally. The expression of proenkephalin was decreased in cancers from patients with advanced disease. Inhibition of secretogranin-II expression decreased the secretory response to IGF, and its over-expression recovered the secretory response consistent with a role in secretory vesicle biogenesis. We conclude that normal and some gastric cancer myofibroblasts have a neuroendocrine-like phenotype characterized by Ca(2+)-dependent regulated secretion, dense-core secretory vesicles and expression of neuroendocrine marker proteins; loss of the phenotype is associated with advanced cancer. A failure to regulate myofibroblast protein secretion may contribute to cancer progression.
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Registered trials
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