ArticleOncotarget2015
V-ATPase: a master effector of E2F1-mediated lysosomal trafficking, mTORC1 activation and autophagy.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- ATP6V0B promotes the tumorigenesis of bladder cancer by activating PAQR4/PI3K/AKT signaling.BMC cancer · 2025Article
- Mitochondrial phosphoenolpyruvate carboxykinase promotes tumor growth in estrogen receptor-positive breast cancer via regulation of the mTOR pathway.Cancer medicine · 2023Article
- MEK/ERK-mediated oncogenic signals promote secretion of extracellular vesicles by controlling lysosome function.Cancer science · 2022Article
- Circular RNA circ-FoxO3 attenuates blood-brain barrier damage by inducing autophagy during ischemia/reperfusion.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Hypoxia-stimulated ATM activation regulates autophagy-associated exosome release from cancer-associated fibroblasts to promote cancer cell invasion.Journal of extracellular vesicles · 2021Article
- The multifaceted role of cell cycle regulators in the coordination of growth and metabolism.The FEBS journal · 2021Review
- Perspectives on Organelle Interaction, Protein Dysregulation, and Cancer Disease.Frontiers in cell and developmental biology · 2021Review
- Protein Homeostasis Networks and the Use of Yeast to Guide Interventions in Alzheimer's Disease.International journal of molecular sciences · 2020Review
- Article
- A modified lysosomal organelle mediates nonlytic egress of reovirus.The Journal of cell biology · 2020Article
- Autophagy Roles in Genome Maintenance.Cancers · 2020Review
- Effects of Environmental pH on the Growth of Gastric Cancer Cells.Gastroenterology research and practice · 2020Article
- How does mTOR sense glucose starvation? AMPK is the usual suspect.Cell death discovery · 2020Review
- Lipid droplet velocity is a microenvironmental sensor of aggressive tumors regulated by V-ATPase and PEDF.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Phosphofructokinases Axis Controls Glucose-Dependent mTORC1 Activation Driven by E2F1.iScience · 2019Article
- CDK4 Regulates Lysosomal Function and mTORC1 Activation to Promote Cancer Cell Survival.Cancer research · 2019Article
- Loss of Sirtuin 1 Alters the Secretome of Breast Cancer Cells by Impairing Lysosomal Integrity.Developmental cell · 2019Article
- The Importance of mTOR Trafficking for Human Skeletal Muscle Translational Control.Exercise and sport sciences reviews · 2019Review
- mTORC1 and Nutrient Homeostasis: The Central Role of the Lysosome.International journal of molecular sciences · 2018Review
- Systems biology analysis of longitudinal functional response of endothelial cells to shear stress.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to being a master regulator of cell cycle progression, E2F1 regulates other associated biological processes, including growth and malignancy. Here, we uncover a regulatory network linking E2F1 to lysosomal trafficking and mTORC1 signaling that involves v-ATPase regulation. By immunofluorescence and time-lapse microscopy we found that E2F1 induces the movement of lysosomes to the cell periphery, and that this process is essential for E2F1-induced mTORC1 activation and repression of autophagy. Gain- and loss-of-function experiments reveal that E2F1 regulates v-ATPase activity and inhibition of v-ATPase activity repressed E2F1-induced lysosomal trafficking and mTORC1 activation. Immunoprecipitation experiments demonstrate that E2F1 induces the recruitment of v-ATPase to lysosomal RagB GTPase, suggesting that E2F1 regulates v-ATPase activity by enhancing the association of V0 and V1 v-ATPase complex. Analysis of v-ATPase subunit expression identified B subunit of V0 complex, ATP6V0B, as a transcriptional target of E2F1. Importantly, ATP6V0B ectopic-expression increased v-ATPase and mTORC1 activity, consistent with ATP6V0B being responsible for mediating the effects of E2F1 on both responses. Our findings on lysosomal trafficking, mTORC1 activation and autophagy suppression suggest that pharmacological intervention at the level of v-ATPase may be an efficacious avenue for the treatment of metastatic processes in tumors overexpressing E2F1.
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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.