ArticleCell communication and signaling : CCS2014
Inflammation and pancreatic cancer: molecular and functional interactions between S100A8, S100A9, NT-S100A8 and TGFβ1.
Article in Cell communication and signaling : CCS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 36 citations in OpenAlex.
- Interleukin-1α (IL-1α) in pancreatic ductal adenocarcinoma: implications for immunotherapy and molecular biomarkers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Article
- The role of S100A8 and S100A9 in external auditory canal cholesteatoma.Frontiers in immunology · 2024Article
- S100a9 inhibits Atg9a transcription and participates in suppression of autophagy in cardiomyocytes induced by βCellular & molecular biology letters · 2023Article
- Eliminating the invading extracellular and intracellular FnBpFrontiers in cellular and infection microbiology · 2023Article
- The functions and regulatory pathways of S100A8/A9 and its receptors in cancers.Frontiers in pharmacology · 2023Review
- Resistance to Gemcitabine in Pancreatic Ductal Adenocarcinoma: A Physiopathologic and Pharmacologic Review.Cancers · 2022Review
- Identification of differentially expressed proteins involved in fetal scarless wound healing using a rat model of cleft lip.Molecular medicine reports · 2021Article
- Review
- Identification of EMT signaling cross-talk and gene regulatory networks by single-cell RNA sequencing.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Targeting Fibrosis: The Bridge That Connects Pancreatitis and Pancreatic Cancer.International journal of molecular sciences · 2021Review
- S100A8 transported by SEC23A inhibits metastatic colonization via autocrine activation of autophagy.Cell death & disease · 2020Article
- Local and systemic immunosuppression in pancreatic cancer: Targeting the stalwarts in tumor's arsenal.Biochimica et biophysica acta. Reviews on cancer · 2020Review
- Comparative proteomes change and possible role in different pathways of microRNA-21a-5p in a mouse model of spinal cord injury.Neural regeneration research · 2020Article
- Article
- Inflammation and Pancreatic Cancer: Focus on Metabolism, Cytokines, and Immunity.International journal of molecular sciences · 2019Review
- Serum amyloid A1 in combination with integrin αVβ3 increases glioblastoma cells mobility and progression.Molecular oncology · 2018Article
- S100A9 gene silencing inhibits the release of pro-inflammatory cytokines by blocking the IL-17 signalling pathway in mice with acute pancreatitis.Journal of cellular and molecular medicine · 2018Article
- Protein S100-A8: A potential metastasis-associated protein for breast cancer determined via iTRAQ quantitative proteomic and clinicopathological analysis.Oncology letters · 2018Article
- Inhibition of Expression of the S100A8 Gene Encoding the S100 Calcium-Binding Protein A8 Promotes Apoptosis by Suppressing the Phosphorylation of Protein Kinase B (Akt) in Endometrial Carcinoma and HEC-1A Cells.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn order to gain further insight on the crosstalk between pancreatic cancer (PDAC) and stromal cells, we investigated interactions occurring between TGFβ1 and the inflammatory proteins S100A8, S100A9 and NT-S100A8, a PDAC-associated S100A8 derived peptide, in cell signaling, intracellular calcium (Cai2+) and epithelial to mesenchymal transition (EMT). NF-κB, Akt and mTOR pathways, Cai2+ and EMT were studied in well (Capan1 and BxPC3) and poorly differentiated (Panc1 and MiaPaCa2) cell lines.
resultsNT-S100A8, one of the low molecular weight N-terminal peptides from S100A8 to be released by PDAC-derived proteases, shared many effects on NF-κB, Akt and mTOR signaling with S100A8, but mainly with TGFβ1. The chief effects of S100A8, S100A9 and NT-S100A8 were to inhibit NF-κB and stimulate mTOR; the molecules inhibited Akt in Smad4-expressing, while stimulated Akt in Smad4 negative cells. By restoring Smad4 expression in BxPC3 and silencing it in MiaPaCa2, S100A8 and NT-S100A8 were shown to inhibit NF-κB and Akt in the presence of an intact TGFβ1 canonical signaling pathway. TGFβ1 counteracted S100A8, S100A9 and NT-S100A8 effects in Smad4 expressing, not in Smad4 negative cells, while it synergized with NT-S100A8 in altering Cai2+ and stimulating PDAC cell growth. The effects of TGFβ1 on both EMT (increased Twist and decreased N-Cadherin expression) and Cai2+ were antagonized by S100A9, which formed heterodimers with TGFβ1 (MALDI-TOF/MS and co-immuno-precipitation).
conclusionsThe effects of S100A8 and S100A9 on PDAC cell signaling appear to be cell-type and context dependent. NT-S100A8 mimics the effects of TGFβ1 on cell signaling, and the formation of complexes between TGFβ1 with S100A9 appears to be the molecular mechanism underlying the reciprocal antagonism of these molecules on cell signaling, Cai2+ and EMT.
Indexed as
Identifiers
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.