ArticleCell death discovery2023
S100A2 induces epithelial-mesenchymal transition and metastasis in pancreatic cancer by coordinating transforming growth factor β signaling in SMAD4-dependent manner.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
- Crosstalk between KRAS and miRNAs in pancreatic cancer: Opportunities for its diagnosis, prognosis and therapeutic intervention (Review).International journal of oncology · 2026Review
- From Pyroptosis Heterogeneity to an Interpretable Prognostic Signature for Risk Stratification and Therapy Insights in Pancreatic Adenocarcinoma.Biomedicines · 2026Article
- Spatial Distribution of K13-Positive Airway Epithelial Cells in Idiopathic Pulmonary Fibrosis.Biomedicines · 2026Article
- HDAC6 orchestrates metastatic and immunosuppressive programs in small cell lung cancer through S100A2-TGF-β/SMAD and CSF1R signaling.Molecular cancer · 2026Article
- Quercetin and 5-Fluorouracil Synergistically Suppress ZEB1 and Restore Epithelial Integrity in Triple-Negative Breast Cancer.Iranian biomedical journal · 2026Article
- Recent advances in hydrogel-based delivery systems for the treatment of pancreatic cancer.Materials today. Bio · 2025Review
- Role of S100 family proteins in colorectal cancer (CRC): an overview of their potential function as new biomarkers and therapeutic agents.Expert reviews in molecular medicine · 2025Review
- INHBABMC cancer · 2025Article
- A Mutual Interaction Between GSTP1 and p53 Improves the Drug Resistance and Malignant Biology of Pancreatic Cancer.Cancer science · 2025Article
- The scRNA-sequencing landscape of pancreatic ductal adenocarcinoma revealed distinct cell populations associated with tumor initiation and progression.Genes & diseases · 2025Article
- Prognostic and immunotherapeutic potential of disulfidptosis-associated signature in pancreatic cancer.Frontiers in immunology · 2025Article
- S100A2 activation promotes interstitial fibrosis in kidneys by FoxO1-mediated epithelial-mesenchymal transition.Cell biology and toxicology · 2024Article
- Harnessing Plant Flavonoids to Fight Pancreatic Cancer.Current nutrition reports · 2024Review
- Induction of Cell Death byJournal of microbiology and biotechnology · 2024Article
- Linderapyrone analogue LPD-01 as a cancer treatment agent by targeting importin7.Journal of natural medicines · 2024Article
- SSPH I, A Novel Anti-cancer Saponin, Inhibits EMT and Invasion and Migration of NSCLC by Suppressing MAPK/ERK1/2 and PI3K/AKT/ mTOR Signaling Pathways.Recent patents on anti-cancer drug discovery · 2024Article
- Overexpression of S100 Calcium-Binding Protein A2 is Associated With Poor Prognosis in Hepatocellular Carcinoma.Cancer control : journal of the Moffitt Cancer CenterArticle
- [Hepatocellular carcinoma-derived lactate-mediated histone H3K18 lactylation modifies S100A2 transcription to promote proliferation, migration, invasion and epithelial-mesenchymal transition of hepatocellular carcinoma cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical UniversityArticle
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive tumor and is associated with a poor prognosis. Treatment strategies for PDAC are largely ineffective primarily because of delay in its diagnosis and limited efficacy of systematic treatment. S100A2 is associated with the proliferation, migration, and differentiation of several tumors; however, its effects on PDAC and the associated molecular mechanisms remain to be explored. We studied the mechanisms underlying the effect of S100A2 on epithelial-mesenchymal transition (EMT) and metastasis in PDAC cells. We found that the level of S100A2 remarkably increased and was associated with poor PDAC prognosis. The overexpression of S100A2 in PANC-1 cells also induced EMT, in addition to increasing the invasion and migration of PDAC cells, whereas the knockdown of S100A2 markedly inhibited cell metastasis. Furthermore, S100A2 was found to enhance metastatic abilities in vivo. The overexpression of S100A2 increased SMAD4 expression, whereas the knockdown of S100A2 reduced SMAD4 expression. SMAD4 overexpression could effectively rescue the effects of S100A2 knockdown on EMT. S100A2 mechanistically activated the transforming growth factor (TGF)-β/Smad2/3 signaling pathway, upregulated SMAD4 expression, induced EMT, and increased PANC-1 cell metastasis. In conclusion, the S100A2/SMAD4 axis modulates EMT to accelerate PDAC development. Our results supplement and enrich the understanding of the pathogenesis underlying PDAC and provide a new theoretical basis and strategy targeting S100A2 for the diagnosis and treatment of PDAC.
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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.