ArticleWorld journal of gastroenterology2014
Distinct antifibrogenic effects of erlotinib, sunitinib and sorafenib on rat pancreatic stellate cells.
Article in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- Orai1 Channel Regulates Human-Activated Pancreatic Stellate Cell Proliferation and TGFCancers · 2021Article
- Functions of pancreatic stellate cell-derived soluble factors in the microenvironment of pancreatic ductal carcinoma.Oncotarget · 2017Review
- Upregulation of COL6A1 is predictive of poor prognosis in clear cell renal cell carcinoma patients.Oncotarget · 2015Article
- Are biological agents toxic to human chondrocytes and osteocytes?Journal of orthopaedic surgery and research · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo study if three clinically available small molecule kinase inhibitors (SMI), erlotinib, sunitinib and sorafenib, exert antifibrogenic effects on pancreatic stellate cells (PSC) and analyze the basis of their action.
methodsCultured rat PSC were exposed to SMI. Cell proliferation and viability were assessed employing 5-bromo-2'-deoxyuridine incorporation assay and flow cytometry, respectively. 2-Deoxy-2-[(18)F] fluoroglucose ((18)F-FDG) uptake was measured to study metabolic activity. Exhibition of the myofibroblastic PSC phenotype was monitored by immunofluorescence analysis of α-smooth muscle actin (α-SMA) expression. Levels of mRNA were determined by real-time PCR, while protein expression and phosphorylation were analyzed by immunoblotting. Transforming growth factor-β1 (TGF-β1) levels in culture supernatants were quantified by ELISA.
resultsAll three SMI inhibited cell proliferation and (18)F-FDG uptake in a dose-dependent manner and without significant cytotoxic effects. Furthermore, additive effects of the drugs were observed. Immunoblot analysis showed that sorafenib and sunitib, but not erlotinib, efficiently blocked activation of the AKT pathway, while all three drugs displayed little effect on phosphorylation of ERK1/2. Cells treated with sorafenib or sunitinib expressed less interleukin-6 mRNA as well as less collagen type 1 mRNA and protein. Sorafenib was the only drug that also upregulated the expression of matrix metalloproteinase-2 and reduced the secretion of TGF-β1 protein. All three drugs showed insignificant or discordant effects on the mRNA and protein levels of α-SMA.
conclusionThe tested SMI, especially sorafenib, exert inhibitory effects on activated PSC, which should be further evaluated in preclinical studies.
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