ArticleMolecular carcinogenesis2019
S100A11 promotes cell proliferation via P38/MAPK signaling pathway in intrahepatic cholangiocarcinoma.
Article in Molecular carcinogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- Construction and validation of renal cell carcinoma tumor cell differentiation-related prognostic classification (RCC-TCDC): an integrated bioinformatic analysis and clinical study.Annals of medicine · 2025Article
- Relationship of S100 Proteins with Neuroinflammation.Biomolecules · 2025Review
- LiverSCA 2.0: An Enhanced Comprehensive Cell Atlas for Human Hepatocellular Carcinoma and Intrahepatic Cholangiocarcinoma.Cancers · 2025Article
- Identification of new biomarkers of hepatic cancer stem cells through proteomic profiling.Journal of liver cancer · 2025Article
- Article
- Exploring Core Genes Associated with Sepsis and Systemic Inflammatory Response Syndrome Using Single-Cell Sequencing Technology.Journal of inflammation research · 2025Article
- Lactylation-driven molecular taxonomy of melanoma: linking epigenetic modifications to immune evasion and clinical outcomes.American journal of cancer research · 2025Article
- S100A11 as an immune-related exosomal driver of colorectal cancer progression: a novel diagnostic biomarker.Frontiers in oncology · 2025Article
- S100A11 is involved in the progression of colorectal cancer through the desmosome-catenin-TCF signaling pathway.In vitro cellular & developmental biology. Animal · 2024Article
- Article
- Exploring the prognostic value of S100A11 and its association with immune infiltration in breast cancer.Scientific reports · 2023Article
- S100A11 Promotes Metastasis via AKT and ERK Signaling Pathways and Has a Diagnostic Role in Hepatocellular Carcinoma.International journal of medical sciences · 2023Article
- S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma.International journal of molecular sciences · 2022Review
- Curcuminoids as Modulators of EMT in Invasive Cancers: A Review of Molecular Targets With the Contribution of Malignant Mesothelioma Studies.Frontiers in pharmacology · 2022Review
- Downregulation of MCM8 expression restrains the malignant progression of cholangiocarcinoma.Oncology reports · 2021Article
- GSG2 knockdown suppresses cholangiocarcinoma progression by regulating cell proliferation, apoptosis and migration.Oncology reports · 2021Article
- The Calcium Binding Protein S100A11 and Its Roles in Diseases.Frontiers in cell and developmental biology · 2021Review
- Article
- Mass spectrometry-based analysis of formalin-fixed, paraffin-embedded distal cholangiocarcinoma identifies stromal thrombospondin-2 as a potential prognostic marker.Journal of translational medicine · 2020Article
- Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
Abstract
S100A11 is reported to associate with progression and poor prognosis in several tumors. We previously reported that S100A11 was highly expressed in intrahepatic cholangiocarcinoma (ICC) cells and promoted TGF-β1-induced EMT through SMAD2/3 signaling pathway. Here, we explored the prognostic role of S100A11 on ICC patients and preliminary molecular mechanisms how S100A11 regulated ICC cell proliferation. Our results showed that S100A11 was obviously increased in ICC tumor tissues. High expression of S100A11 was closely correlated with lymph node metastasis (LNM) and TNM stage and was an independent risk factor for patients' overall survival (OS) and recurrence-free survival (RFS). The nomograms comprising LNM and S100A11 achieved better predictive accuracy compared with TNM staging system for OS and RFS prediction. Silencing S100A11 significantly suppressed RBE cells and HCCC9810 cells proliferation, colony formation, and activation of P38/mitogen-activated protein kinase (MAPK) signaling pathway in vitro and inhibited tumor growth in vivo. In contrast, the overexpression of S100A11 in RBE cells and HCCC9810 cells achieved the opposite results. S100A11-induced proliferation was abolished after treatment with P38 inhibitor. Our findings suggest S100A11/P38/MAPK signaling pathway may be a potential therapeutic target for ICC patients.
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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.