ArticleNature communications2020
Macropinocytosis confers resistance to therapies targeting cancer anabolism.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.
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.
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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
107 citing papers in PubMed, 196 citations in OpenAlex.
- Enhanced anticancer efficacy ofMaterials today. Bio · 2026Article
- MSC EVs Deliver miRNAs into Cardiomyocytes via EIPA-Sensitive and Clathrin-Mediated Endocytosis.Biomedicines · 2026Article
- DHODH inhibition drives albumin-mediated drug resistance through TERF2IP lactylation-activated macropinosome-mitochondria contact.Nature communications · 2026Article
- Bioengineered systems to exploit tumor microenvironment metabolism.Trends in cancer · 2026Review
- Exploiting Macropinocytosis Drives Redox Vulnerability to Preferentially Target Drug-Resistant Cancer.ACS nano · 2026Article
- Advances in delivery technologies-powered cancer vaccines.Bioactive materials · 2026Review
- Metabolic plasticity in pancreatic ductal adenocarcinoma progression and response to treatment.Molecular cancer · 2026Review
- Article
- Targeting macropinocytosis for cancer therapy.Nature reviews. Cancer · 2026Review
- NF2 loss malignantly transforms human pancreatic acinar cells and enhances cell fitness under environmental stress.The Journal of clinical investigation · 2026Article
- A Holistic Review of Oncological Drug Targets and Trajectories of Resistance in Cancer Therapy.Oncology research · 2026Review
- Aldolase a coordinates macropinocytic nutrient scavenging and lysosomal degradation in lung cancer by interacting with V-ATPase.Cell communication and signaling : CCS · 2025Article
- Targeting autophagy in dysfunctional tumor vasculature.iScience · 2025Review
- SLC6A14-mediated glutamine promotes SYTL4-CXCL8 axis activation to drive gemcitabine resistance and immune evasion in pancreatic cancer.Experimental & molecular medicine · 2025Article
- Impairment of Hyaluronan-Related Glycocalyx Inhibits Macropinocytosis in Cancer Cells via p21 Upregulation.Biomacromolecules · 2025Article
- Cascade-Targeted Nanoparticles for Enhanced Gemcitabine Delivery and Adenosine Metabolism Modulation to Overcome Treatment Resistance in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Tuning probe permeabilityChemical science · 2025Article
- Lysosome-dependent nutrient scavenging underlies stress adaptation during epithelial-to-mesenchymal transition.bioRxiv : the preprint server for biology · 2025Article
- Macropinocytosis maintains CAF subtype identity under metabolic stress in pancreatic cancer.Cancer cell · 2025Article
- Hyperlipidemia drives tumor growth in a mouse model of obesity-accelerated breast cancer growth.Cancer & metabolism · 2025Article
47 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Macropinocytic cancer cells scavenge amino acids from extracellular proteins. Here, we show that consuming necrotic cell debris via macropinocytosis (necrocytosis) offers additional anabolic benefits. A click chemistry-based flux assay reveals that necrocytosis provides not only amino acids, but sugars, fatty acids and nucleotides for biosynthesis, conferring resistance to therapies targeting anabolic pathways. Indeed, necrotic cell debris allow macropinocytic breast and prostate cancer cells to proliferate, despite fatty acid synthase inhibition. Standard therapies such as gemcitabine, 5-fluorouracil (5-FU), doxorubicin and gamma-irradiation directly or indirectly target nucleotide biosynthesis, creating stress that is relieved by scavenged nucleotides. Strikingly, necrotic debris also render macropinocytic, but not non-macropinocytic, pancreas and breast cancer cells resistant to these treatments. Selective, genetic inhibition of macropinocytosis confirms that necrocytosis both supports tumor growth and limits the effectiveness of 5-FU in vivo. Therefore, this study establishes necrocytosis as a mechanism for drug resistance.
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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.