ArticleOncotarget2017
Rab7 GTPase controls lipid metabolic signaling in myeloid-derived suppressor cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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
23 citing papers in PubMed, 34 citations in OpenAlex.
- Abnormal fat distribution in two patients with RAB7A-associated Charcot-Marie-Tooth type 2B: a case report.BMC neurology · 2025Article
- Engineering a cell-based orthogonal ubiquitin transfer cascade for profiling the substrates of RBR E3 Parkin.iScience · 2025Article
- The role of sirtuins in the regulation of reactive oxygen species in myocardial ischemia/reperfusion injury.Molecular and cellular biochemistry · 2025Review
- Induced mitochondrial deficit by NDUFS3 transient silencing reduces RAB7 expression and causes lysosomal dysfunction in pancreatic cancer cells.Cell communication and signaling : CCS · 2025Article
- The interrelated roles of RAB family proteins in the advancement of neoplastic growth.Frontiers in oncology · 2025Review
- Endosomal traffic disorders: a driving force behind neurodegenerative diseases.Translational neurodegeneration · 2024Review
- Defects of mitochondria-lysosomes communication induce secretion of mitochondria-derived vesicles and drive chemoresistance in ovarian cancer cells.Cell communication and signaling : CCS · 2024Article
- Remodeling the tumor immune microenvironment via siRNA therapy for precision cancer treatment.Asian journal of pharmaceutical sciences · 2023Review
- The regulatory role of lipophagy in central nervous system diseases.Cell death discovery · 2023Review
- Review
- Linking Late Endosomal Cholesterol with Cancer Progression and Anticancer Drug Resistance.International journal of molecular sciences · 2022Review
- Metabolic reprograming of MDSCs within tumor microenvironment and targeting for cancer immunotherapy.Acta pharmacologica Sinica · 2022Review
- Danshensu Ameliorates Cardiac Ischaemia Reperfusion Injury through Activating Sirt1/FoxO1/Rab7 Signal Pathway.Chinese journal of integrative medicine · 2020Article
- The Functional Impact of Mitochondrial Structure Across Subcellular Scales.Frontiers in physiology · 2020Review
- Neutrophil Metabolic Shift during their Lifecycle: Impact on their Survival and Activation.International journal of molecular sciences · 2019Review
- Metabolic implications of organelle-mitochondria communication.EMBO reports · 2019Review
- Review
- Metabolic and functional reprogramming of myeloid-derived suppressor cells and their therapeutic control in glioblastoma.Cell stress · 2019Review
- Degradation of dendritic cargos requires Rab7-dependent transport to somatic lysosomes.The Journal of cell biology · 2018Article
- Autophagy orchestrates the regulatory program of tumor-associated myeloid-derived suppressor cells.The Journal of clinical investigation · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Lysosomal acid lipase (LAL) is a critical neutral lipid metabolic enzyme that regulates metabolic reprogramming in myeloid-derived suppressor cells (MDSCs) through over-activation of mammalian target of rapamycin (mTOR). Affymetrix GeneChip microarray analysis of MDSCs from LAL deficient mouse (lal-/-) revealed upregulation of Rab7 GTPase protein, which belongs to a superfamily of small-molecular-weight GTPase known to regulate intracellular membrane trafficking from early to late endosomes and lysosomes. Here, the physical protein-protein interaction between Rab7 GTPase and mTOR has been detected by co-immunoprecipitation in the cell extract of wild type HD1A and lal-/- MDSC-like HD1B myeloid cell lines. The GST pull down assay using the recombinant GST-Rab7 GTPase fusion protein showed that Rab7 GTPase interacts with the mTOR N-terminal heat repeat domain. Rab7 GTPase siRNA knocking down reversed the altered lysosome/mTOR distribution and expression levels in HD1B cells. Rab7 GTPase siRNA knocking down in isolated bone marrow lal-/- MDSCs or HD1B cells not only reduced over-activation of mTOR and its downstream effector S6, but also decreased glucose consumption, decreased ROS over-production, and increased healthy mitochondria by membrane potential measurement. Inhibition of Rab7 GTPase led to reduced lal-/- MDSCs differentiation from bone marrow Lin- progenitor cells, reduced lal-/- MDSCs trans-endothelial migration, and reversed lal-/- MDSCs suppression of T cell proliferation. Furthermore, inhibition of Rab7 GTPase reduced lal-/- MDSCs ability to stimulate tumor cell proliferation in vitro, tumor growth in vivo, and tumor invasion. Together, these results showed that Rab7 GTPase is critically involved in MDSCs homeostasis and pathogenic functions.
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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.