ArticleProceedings of the National Academy of Sciences of the United States of America2016
Macroautophagy is dispensable for growth of KRAS mutant tumors and chloroquine efficacy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 2 of them syntheses that pooled it.
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Who cites it
151 citing papers in PubMed, 2 syntheses or guidelines pooled it, 221 citations in OpenAlex.
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- Pooled it
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- Autophagy modulation in cancer.Nature reviews. Drug discovery · 2026Review
- Oxidative stress induced by DMSA-IONPs impairs breast cancer cell migration and paracrine cell communication.Journal of nanobiotechnology · 2026Article
- Article
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- An overview of autophagy inhibition as a potential clinical strategy in cancer therapy.Molecular pharmacology · 2025Review
- Differential regulation of STING expression and cisplatin sensitivity by autophagy in non-small cell lung cancer cells.Medical oncology (Northwood, London, England) · 2025Article
- Quantitative profiling pH heterogeneity of acidic endolysosomal compartments using fluorescence lifetime imaging microscopy.Molecular biology of the cell · 2025Article
- Inhibition of autophagy as a novel treatment for neurofibromatosis type 1 tumors.Molecular oncology · 2025Article
- Crosstalk Between Autophagy and Oxidative Stress in Hematological Malignancies: Mechanisms, Implications, and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- Research for a Common Thread: Insights into the Mechanisms of Six Potential Anticancer Agents.Molecules (Basel, Switzerland) · 2025Article
- Targeting secretory autophagy in solid cancers: mechanisms, immune regulation and clinical insights.Experimental hematology & oncology · 2025Review
- Autophagy as a potential therapeutic target in regulating improper cellular proliferation.Frontiers in pharmacology · 2025Review
- Innate immune and endoplasmic reticulum unfolded protein response pathways protectJournal of biosciences · 2025Article
- LOC730101 improves ovarian cancer drug sensitivity by inhibiting autophagy-mediated DNA damage repair via BECN1.Cell death & disease · 2024Article
- Promising and challenging phytochemicals targeting LC3 mediated autophagy signaling in cancer therapy.Immunity, inflammation and disease · 2024Review
- Rationally designed catalytic nanoplatform for enhanced chemoimmunotherapy via deploying endogenous plus exogenous copper and remodeling tumor microenvironment.Journal of nanobiotechnology · 2024Article
91 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macroautophagy is a key stress-response pathway that can suppress or promote tumorigenesis depending on the cellular context. Notably, Kirsten rat sarcoma (KRAS)-driven tumors have been reported to rely on macroautophagy for growth and survival, suggesting a potential therapeutic approach of using autophagy inhibitors based on genetic stratification. In this study, we evaluated whether KRAS mutation status can predict the efficacy to macroautophagy inhibition. By profiling 47 cell lines with pharmacological and genetic loss-of-function tools, we were unable to confirm that KRAS-driven tumor lines require macroautophagy for growth. Deletion of autophagy-related 7 (ATG7) by genome editing completely blocked macroautophagy in several tumor lines with oncogenic mutations in KRAS but did not inhibit cell proliferation in vitro or tumorigenesis in vivo. Furthermore, ATG7 knockout did not sensitize cells to irradiation or to several anticancer agents tested. Interestingly, ATG7-deficient and -proficient cells were equally sensitive to the antiproliferative effect of chloroquine, a lysosomotropic agent often used as a pharmacological tool to evaluate the response to macroautophagy inhibition. Moreover, both cell types manifested synergistic growth inhibition when treated with chloroquine plus the tyrosine kinase inhibitors erlotinib or sunitinib, suggesting that the antiproliferative effects of chloroquine are independent of its suppressive actions on autophagy.
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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.