ArticleMolecular biology of the cell2012
Quiescent fibroblasts are protected from proteasome inhibition-mediated toxicity.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- Transcription factor networks in cellular quiescence.Nature cell biology · 2025Review
- The canonical E2Fs together with RETINOBLASTOMA-RELATED are required to establish quiescence during plant development.Communications biology · 2023Article
- Mitochondrial respiratory quiescence: A new model for examining the role of mitochondrial metabolism in development.Seminars in cell & developmental biology · 2023Review
- Mitochondrial respiration supports autophagy to provide stress resistance during quiescence.Autophagy · 2022Article
- Adult fibroblasts use aggresomes only in distinct cell-states.Scientific reports · 2022Article
- ROS-induced cell cycle arrest as a mechanism of resistance in polyaneuploid cancer cells (PACCs).Progress in biophysics and molecular biology · 2021Article
- Skeletal Aging and Osteoporosis: Mechanisms and Therapeutics.International journal of molecular sciences · 2021Review
- Is There a Histone Code for Cellular Quiescence?Frontiers in cell and developmental biology · 2021Review
- A Mouse Model to Investigate the Role of Cancer-associated Fibroblasts in Tumor Growth.Journal of visualized experiments : JoVE · 2020Article
- Serum deprivation initiates adaptation and survival to oxidative stress in prostate cancer cells.Scientific reports · 2020Article
- Regulation of Cell Cycle Entry and Exit: A Single Cell Perspective.Comprehensive Physiology · 2019Review
- Alternative polyadenylation factors link cell cycle to migration.Genome biology · 2018Article
- Drug repurposing screening identifies bortezomib and panobinostat as drugs targeting cancer associated fibroblasts (CAFs) by synergistic induction of apoptosis.Investigational new drugs · 2018Article
- Exit from quiescence displays a memory of cell growth and division.Nature communications · 2017Article
- An Exportin-1-dependent microRNA biogenesis pathway during human cell quiescence.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Elimination of quiescent slow-cycling cells via reducing quiescence depth by natural compounds purified from Ganoderma lucidum.Oncotarget · 2017Article
- Cell cycle proliferation decisions: the impact of single cell analyses.The FEBS journal · 2017Review
- Prolonged proteasome inhibition cyclically upregulates Oct3/4 and Nanog gene expression, but reduces induced pluripotent stem cell colony formation.Cellular reprogramming · 2015Article
- A high ratio of G1 to G0 phase cells and an accumulation of G1 phase cells before S phase progression after injurious stimuli in the proximal tubule.Physiological reports · 2014Article
- Assessing subunit dependency of the Plasmodium proteasome using small molecule inhibitors and active site probes.ACS chemical biology · 2014Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Proteasome inhibition is used as a treatment strategy for multiple types of cancers. Although proteasome inhibition can induce apoptotic cell death in actively proliferating cells, it is less effective in quiescent cells. In this study, we used primary human fibroblasts as a model system to explore the link between the proliferative state of a cell and proteasome inhibition-mediated cell death. We found that proliferating and quiescent fibroblasts have strikingly different responses to MG132, a proteasome inhibitor; proliferating cells rapidly apoptosed, whereas quiescent cells maintained viability. Moreover, MG132 treatment of proliferating fibroblasts led to increased superoxide anion levels, juxtanuclear accumulation of ubiquitin- and p62/SQSTM1-positive protein aggregates, and apoptotic cell death, whereas MG132-treated quiescent cells displayed fewer juxtanuclear protein aggregates, less apoptosis, and higher levels of mitochondrial superoxide dismutase. In both cell states, reducing reactive oxygen species with N-acetylcysteine lessened protein aggregation and decreased apoptosis, suggesting that protein aggregation promotes apoptosis. In contrast, increasing cellular superoxide levels with 2-methoxyestradiol treatment or inhibition of autophagy/lysosomal pathways with bafilomycin A1 sensitized serum-starved quiescent cells to MG132-induced apoptosis. Thus, antioxidant defenses and the autophagy/lysosomal pathway protect serum-starved quiescent fibroblasts from proteasome inhibition-induced cytotoxicity.
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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.