ArticleThe Journal of biological chemistry2014
The transcription factor GLI1 modulates the inflammatory response during pancreatic tissue remodeling.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 54 citations in OpenAlex.
- Wilms Tumor 1-Expressing Stromal Cells Promote Pancreatic Cancer Progression.Cancer research · 2026Article
- KRAS Mutations in Cancer: Understanding Signaling Pathways to Immune Regulation and the Potential of Immunotherapy.Cancers · 2025Review
- Pharmacologic Hedgehog inhibition modulates the cytokine profile of osteolytic breast cancer cells.Journal of bone oncology · 2024Article
- Endoplasmic reticulum aminopeptidase 2 regulates CD4Arthritis research & therapy · 2024Article
- Characterizing hedgehog pathway features in senescence associated osteoarthritis through Integrative multi-omics and machine learning analysis.Frontiers in genetics · 2024Article
- SUFU promotes GLI activity in a Hedgehog-independent manner in pancreatic cancer.The Biochemical journal · 2023Article
- Identifying Fibrogenic Cells Following Salivary Gland Obstructive Injury.bioRxiv : the preprint server for biology · 2023Article
- Inhibition of GPR39 restores defects in endothelial cell-mediated neovascularization under the duress of chronic hyperglycemia: Evidence for regulatory roles of the sonic hedgehog signaling axis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Identifying fibrogenic cells following salivary gland obstructive injury.Frontiers in cell and developmental biology · 2023Article
- Combinatorial Gli activity directs immune infiltration and tumor growth in pancreatic cancer.PLoS genetics · 2022Article
- The biology of pancreatic cancer morphology.Pathology · 2022Review
- Extrinsic KRAS Signaling Shapes the Pancreatic Microenvironment Through Fibroblast Reprogramming.Cellular and molecular gastroenterology and hepatology · 2022Article
- CD47-Mediated Hedgehog/SMO/GLI1 Signaling Promotes Mesenchymal Stem Cell Immunomodulation in Mouse Liver Inflammation.Hepatology (Baltimore, Md.) · 2021Article
- Gain-of-function p53Cell reports · 2021Article
- Functional crosstalk between myeloid Foxo1-β-catenin axis and Hedgehog/Gli1 signaling in oxidative stress response.Cell death and differentiation · 2021Article
- Pancreatic Cancer and Therapy: Role and Regulation of Cancer Stem Cells.International journal of molecular sciences · 2021Review
- Inhibition of Hedgehog Signaling Alters Fibroblast Composition in Pancreatic Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Diversity and Biology of Cancer-Associated Fibroblasts.Physiological reviews · 2021Review
- Therapeutic Potential of Targeting Stromal Crosstalk-Mediated Immune Suppression in Pancreatic Cancer.Frontiers in oncology · 2021Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Pancreatic cancer, one of the deadliest human malignancies, is almost uniformly associated with a mutant, constitutively active form of the oncogene Kras. Studies in genetically engineered mouse models have defined a requirement for oncogenic KRAS in both the formation of pancreatic intraepithelial neoplasias, the most common precursor lesions to pancreatic cancer, and in the maintenance and progression of these lesions. Previous work using an inducible model allowing tissue-specific and reversible expression of oncogenic Kras in the pancreas indicates that inactivation of this GTPase at the pancreatic intraepithelial neoplasia stage promotes pancreatic tissue repair. Here, we extend these findings to identify GLI1, a transcriptional effector of the Hedgehog pathway, as a central player in pancreatic tissue repair upon Kras inactivation. Deletion of a single allele of Gli1 results in improper stromal remodeling and perdurance of the inflammatory infiltrate characteristic of pancreatic tumorigenesis. Strikingly, this partial loss of Gli1 affects activated fibroblasts in the pancreas and the recruitment of immune cells that are vital for tissue recovery. Analysis of the mechanism using expression and chromatin immunoprecipitation assays identified a subset of cytokines, including IL-6, mIL-8, Mcp-1, and M-csf (Csf1), as direct GLI1 target genes potentially mediating this phenomenon. Finally, we demonstrate that canonical Hedgehog signaling, a known regulator of Gli1 activity, is required for pancreas recovery. Collectively, these data delineate a new pathway controlling tissue repair and highlight the importance of GLI1 in regulation of the pancreatic microenvironment during this cellular process.
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.