ArticleDigestive diseases and sciences2016
IL-6/STAT3 Plays a Regulatory Role in the Interaction Between Pancreatic Stellate Cells and Cancer Cells.
Article in Digestive diseases and sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Immune checkpoint inhibition for pancreatic ductal adenocarcinoma: limitations and prospects: a systematic review.Cell communication and signaling : CCS · 2021Pooled it
- Exosome-mediated regulation of the immune microenvironment via JAK/STAT signaling promotes pancreatic cancer progression.Translational cancer research · 2026Article
- Bottom-Up Programming of Cell States in Cancer Organoids with Defined Synthetic Adhesion Cues.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Focus on Pancreatic Cancer Microenvironment.Current oncology (Toronto, Ont.) · 2024Review
- IL-15-secreting CAR natural killer cells directed toward the pan-cancer target CD70 eliminate both cancer cells and cancer-associated fibroblasts.Journal of hematology & oncology · 2024Article
- Histone Modifications Represent a Key Epigenetic Feature of Epithelial-to-Mesenchyme Transition in Pancreatic Cancer.International journal of molecular sciences · 2023Review
- Low preoperative skeletal muscle index increases the risk of mortality among resectable pancreatic cancer patients: A retrospective study.World journal of gastrointestinal surgery · 2022Article
- Resistance to Gemcitabine in Pancreatic Ductal Adenocarcinoma: A Physiopathologic and Pharmacologic Review.Cancers · 2022Review
- Piezo1-mediated stellate cell activation causes pressure-induced pancreatic fibrosis in mice.JCI insight · 2022Article
- Chemotherapy: a double-edged sword in cancer treatment.Cancer immunology, immunotherapy : CII · 2022Review
- Review
- Targeting Epithelial-to-Mesenchymal Transition in Radioresistance: Crosslinked Mechanisms and Strategies.Frontiers in oncology · 2022Review
- Article
- N-acetyl cysteine induces quiescent-like pancreatic stellate cells from an active state and attenuates cancer-stroma interactions.Journal of experimental & clinical cancer research : CR · 2021Article
- The inhibitory effect of TU-100 on hepatic stellate cell activation in the tumor microenvironment.Oncotarget · 2020Article
- Stroma secreted IL6 selects for "stem-like" population and alters pancreatic tumor microenvironment by reprogramming metabolic pathways.Cell death & disease · 2020Article
- Emerging roles for the IL-6 family of cytokines in pancreatic cancer.Clinical science (London, England : 1979) · 2020Review
- From Genetic Alterations to Tumor Microenvironment: The Ariadne's String in Pancreatic Cancer.Cells · 2020Review
- Activation of STAT3 and STAT5 Signaling in Epithelial Ovarian Cancer Progression: Mechanism and Therapeutic Opportunity.Cancers · 2019Review
- Article
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundPancreatic stellate cells (PSCs) play a pivotal role in pancreatic fibrosis, a characteristic feature of pancreatic cancer. Although it is still controversial, previous studies have suggested that PSCs promote the progression of pancreatic cancer by regulating the cell functions of cancer cells. PSCs produce large amounts of IL-6, which promotes the accumulation of myeloid-derived suppressor cells via a signal transducers and activator of transcription 3 (STAT3)-dependent mechanism. But the role of IL-6/STAT3 pathway in the interaction between PSCs and pancreatic cancer cells remains largely unknown.
aimsTo clarify the role of IL-6/STAT3 in the interaction between PSCs and cancer cells.
methodsHuman pancreatic cancer cells (Panc-1 and SUIT-2 cells) were treated with conditioned medium of immortalized human PSCs (PSC-CM). The effects of PSC-CM and IL-6 neutralization on the mRNA expression profiles were examined using Agilent's microarray. Activation of STAT3 was assessed by Western blotting using an anti-phospho-specific antibody. Cellular migration was examined by a two-chamber assay. The expression of markers related to epithelial-mesenchymal transition (EMT) was assessed by real-time reverse transcription PCR.
resultsPSC-CM induced the activation of STAT3 in pancreatic cancer cells. Neutralization of IL-6 suppressed the PSC-CM-induced upregulation of genes including complement factor B, lipocalin, and chemokine (C-C motif) ligand 20. Inhibition of IL-6/STAT3 pathway by anti-IL-6 antibody or a STAT3 inhibitor (NSC74859) inhibited the PSC-CM-induced migration and the expression of EMT-related markers (Snail and cadherin-2) in pancreatic cancer cells.
conclusionIL-6/STAT3 pathway regulates the PSC-induced EMT and alterations in gene expression in pancreatic cancer cells.
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