ArticleNature2015
Transcriptional control of autophagy-lysosome function drives pancreatic cancer metabolism.
Article in Nature, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 539 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
539 citing papers in PubMed, 1 synthesis or guideline pooled it, 782 citations in OpenAlex.
- Current hotspots and trends in cancer metabolic reprogramming: a scientometric analysis.Frontiers in immunology · 2024Pooled it
- Actinomycetota-Derived Metabolites in Pancreatic Cancer: Chemical Diversity, Metabolic Vulnerability, and Translational Barriers.Current oncology reports · 2026Review
- Article
- Lysosomal metabolism in pancreatic cancer and its crosstalk with host physiology.Genes & development · 2026Review
- Metabolism, autophagy, and cell death: The triangular axis in tumor survival and therapeutic resistance.Redox biology · 2026Review
- Astrocytes mobilize a broader repertoire of lysosomal repair mechanisms than neurons.iScience · 2026Article
- Spiky Magnetic Titania Particles for Integrated Exosome Capture and Metabolic Profiling Toward Cancer Diagnosis.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Targeting lysosome-dependent cell death in cancer: towards therapeutic strategies.Biomarker research · 2026Review
- Periodontitis-Associated Circulating EVs Promote Colorectal Cancer Progression via Carnosine-Mediated Acidosis Adaptation.Cell proliferation · 2026Article
- Lysosomal lipid metabolism promotes tumor cell invasion through local energetics and membrane lipid remodeling.bioRxiv : the preprint server for biology · 2026Article
- The Lysosome-Cathepsin Axis in Pancreatic Cancer: Mechanisms of Stromal Remodeling, Immune Evasion, and Therapy Resistance.Biomolecules · 2026Review
- A comprehensive in silico investigation into the deleterious nonsynonymous single nucleotide polymorphisms of the human transcription factor EB (TFEB) gene and their predicted association with cancer.Journal, genetic engineering & biotechnology · 2026Article
- Loss of UFL1 drives chromosome instability and tumorigenesis of prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Integrated Molecular, Genomic, and Clinical Characterization of Pediatric and Adolescent Translocation Renal Cell Carcinoma: A Report from the Children's Oncology Group.Biomedicines · 2026Article
- Review
- The autophagy-senescence axis as a threshold model of aging and therapeutic targeting.Redox biology · 2026Review
- Second generation PSMA-targeted turn-on probe for imaging cargo release in prostate cancer cells.Bioorganic & medicinal chemistry letters · 2026Article
- Metabolic plasticity in pancreatic ductal adenocarcinoma progression and response to treatment.Molecular cancer · 2026Review
- Article
- Rapid optogenetic manipulation of autophagy reveals that the nuclear pore complex is a robust autophagy substrate.bioRxiv : the preprint server for biology · 2026Article
479 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
Abstract
Activation of cellular stress response pathways to maintain metabolic homeostasis is emerging as a critical growth and survival mechanism in many cancers. The pathogenesis of pancreatic ductal adenocarcinoma (PDA) requires high levels of autophagy, a conserved self-degradative process. However, the regulatory circuits that activate autophagy and reprogram PDA cell metabolism are unknown. Here we show that autophagy induction in PDA occurs as part of a broader transcriptional program that coordinates activation of lysosome biogenesis and function, and nutrient scavenging, mediated by the MiT/TFE family of transcription factors. In human PDA cells, the MiT/TFE proteins--MITF, TFE3 and TFEB--are decoupled from regulatory mechanisms that control their cytoplasmic retention. Increased nuclear import in turn drives the expression of a coherent network of genes that induce high levels of lysosomal catabolic function essential for PDA growth. Unbiased global metabolite profiling reveals that MiT/TFE-dependent autophagy-lysosome activation is specifically required to maintain intracellular amino acid pools. These results identify the MiT/TFE proteins as master regulators of metabolic reprogramming in pancreatic cancer and demonstrate that transcriptional activation of clearance pathways converging on the lysosome is a novel hallmark of aggressive malignancy.
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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.