ArticleNature communications2022
Homophilic ATP1A1 binding induces activin A secretion to promote EMT of tumor cells and myofibroblast activation.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 36 citations in OpenAlex.
- A non-complement role for C1R rewires integrin and death-receptor signaling to drive renal cancer metastasis.Molecular cancer · 2026Article
- PanMETAI - a high performance tabular foundation model for accurate pancreatic cancer diagnosis via NMR metabolomics.Nature communications · 2026Article
- A Proteomic Study of the Dual Oncogenic and Tumor-Suppressive Roles of SIRT3 in Lung and Breast Cancer Cell Lines.International journal of molecular sciences · 2026Article
- Identification, functional insights and therapeutic targeting of EMT tumour states.Nature reviews. Cancer · 2026Review
- Integrative Transcriptomic and Single-Cell Analyses Identify ATP1A1 as a Prognostic and Immune-Associated Factor in Esophageal Cancer.International journal of genomics · 2026Article
- SLC6A14-mediated glutamine promotes SYTL4-CXCL8 axis activation to drive gemcitabine resistance and immune evasion in pancreatic cancer.Experimental & molecular medicine · 2025Article
- LncDARS-AS1 Regulates ATP1A1 Stability and Enhances NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- EGFRvIII-driven microenvironmental fibroblast activation and transformation accelerate oral cancer progression via lipocalin-2/STAT3 axis.Neoplasia (New York, N.Y.) · 2025Article
- Dissecting FAP+ Cell Diversity in Pancreatic Cancer Uncovers an Interferon-Response Subtype of Cancer-Associated Fibroblasts with Tumor-Restraining Properties.Cancer research · 2025Article
- Transcriptomic analysis of laser-capture microdissected tumors reveals RAD51AP1 as a tumor-specific marker associated progression from pancreatic intraepithelial neoplasia to invasive pancreatic cancer.Cancer cell international · 2025Article
- A quantitative spatial cell-cell colocalizations framework enabling comparisons between in vitro assembloids and pathological specimens.Nature communications · 2025Article
- SEMA7A-mediated juxtacrine stimulation of IGFBP-3 upregulates IL-17RB at pancreatic cancer invasive front.Cancer gene therapy · 2024Article
- Barriers and opportunities in pancreatic cancer immunotherapy.NPJ precision oncology · 2024Review
- Activin A plays an essential role in migration and proliferation of hepatic stellate cells via Smad3 and calcium signaling.Scientific reports · 2024Article
- Synthetic control of living cells by intracellular polymerization.Trends in biotechnology · 2024Review
- Gain-of-Function p53 Mutation Acts as a Genetic Switch for TGFβ Signaling-Induced Epithelial-to-Mesenchymal Transition in Intestinal Tumors.Cancer research · 2024Article
- Oncogenic KRAS, Mucin 4, and Activin A-Mediated Fibroblast Activation Cooperate for PanIN Initiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Dihydroartemisinin inhibits liver cancer cell migration and invasion by reducing ATP synthase production through CaMKK2/NCLX.Oncology letters · 2023Article
- Association between high expression of intratumoral fibroblast activation protein and survival in patients with intrahepatic cholangiocarcinoma.BMC gastroenterology · 2023Article
- The role of epithelial-mesenchymal transition and autophagy in pancreatic ductal adenocarcinoma invasion.Cell death & disease · 2023Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor cells with diverse phenotypes and biological behaviors are influenced by stromal cells through secretory factors or direct cell-cell contact. Pancreatic ductal adenocarcinoma (PDAC) is characterized by extensive desmoplasia with fibroblasts as the major cell type. In the present study, we observe enrichment of myofibroblasts in a juxta-tumoral position with tumor cells undergoing epithelial-mesenchymal transition (EMT) that facilitates invasion and correlates with a worse clinical prognosis in PDAC patients. Direct cell-cell contacts forming heterocellular aggregates between fibroblasts and tumor cells are detected in primary pancreatic tumors and circulating tumor microemboli (CTM). Mechanistically, ATP1A1 overexpressed in tumor cells binds to and reorganizes ATP1A1 of fibroblasts that induces calcium oscillations, NF-κB activation, and activin A secretion. Silencing ATP1A1 expression or neutralizing activin A secretion suppress tumor invasion and colonization. Taken together, these results elucidate the direct interplay between tumor cells and bound fibroblasts in PDAC progression, thereby providing potential therapeutic opportunities for inhibiting metastasis by interfering with these cell-cell interactions.
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