ArticleAutophagy2015
Disruption of the ribosomal P complex leads to stress-induced autophagy.
Article in Autophagy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
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Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
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- A label-free microLC-SWATH-MS methodology with immunoaffinity depletion of highly abundant serum proteins for quantitative proteomic comparison of fresh-frozen human normal breast tissue and tumor clinical specimens.Frontiers in molecular biosciences · 2026Article
- RPLP0 identified as a ferroptosis regulator in HCC through pan-cancer analysis.Frontiers in oncology · 2026Article
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- The multifaceted roles of ribosomal P complex in cancer.World journal of surgical oncology · 2025Review
- Mortalin and PINK1/Parkin-Mediated Mitophagy Represent Ovarian Cancer-Selective Targets for Drug Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- TMT-based proteomics analysis identifies RPLP1 as a key protein target in ursolic acid Inhibition of colorectal cancer.Discover oncology · 2025Article
- Targeting RPLP2 Triggers DLBCL Ferroptosis by Decreasing FXN Expression.Biomedicines · 2025Article
- Acrylamide Induces Antiapoptotic Autophagy and Apoptosis by Activating PERK Pathway in SH-SY5Y Cells.Toxics · 2025Article
- Dual PI3K/mTOR inhibitor NVP-BEZ235 induces cell cycle arrest via autophagy mediated protein degradation of RPL19 in nephroblastoma cell.Frontiers in pharmacology · 2025Article
- Adaptation responses to salt stress in the gut ofAnimal cells and systems · 2025Article
- Research Progress of Ribosomal Proteins in Reproductive Development.International journal of molecular sciences · 2024Review
- Multifaceted impact of HIV inhibitor dapivirine on triple negative breast cancer cells reveals potential entities as targets for novel therapy.Scientific reports · 2024Article
- Exploring the function and prognostic value of RPLP0, RPLP1 and RPLP2 expression in lung adenocarcinoma.Journal of molecular histology · 2024Article
- MicroRNA-450b-5p modulated RPLP0 promotes hepatocellular carcinoma progression via activating JAK/STAT3 pathway.Translational oncology · 2024Article
- Ribosomal proteins in hepatocellular carcinoma: mysterious but promising.Cell & bioscience · 2024Review
- Dengue NS1 interaction with lipids alters its pathogenic effects on monocyte derived macrophages.Journal of biomedical science · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human ribosomal P complex, which consists of the acidic ribosomal P proteins RPLP0, RPLP1, and RPLP2 (RPLP proteins), recruits translational factors, facilitating protein synthesis. Recently, we showed that overexpression of RPLP1 immortalizes primary cells and contributes to transformation. Moreover, RPLP proteins are overexpressed in human cancer, with the highest incidence in breast carcinomas. It is thought that disruption of the P complex would directly affect protein synthesis, causing cell growth arrest and eventually apoptosis. Here, we report a distinct mechanism by which cancer cells undergo cell cycle arrest and induced autophagy when RPLP proteins are downregulated. We found that absence of RPLP0, RPLP1, or RPLP2 resulted in reactive oxygen species (ROS) accumulation and MAPK1/ERK2 signaling pathway activation. Moreover, ROS generation led to endoplasmic reticulum (ER) stress that involved the EIF2AK3/PERK-EIF2S1/eIF2α-EIF2S2-EIF2S3-ATF4/ATF-4- and ATF6/ATF-6-dependent arms of the unfolded protein response (UPR). RPLP protein-deficient cells treated with autophagy inhibitors experienced apoptotic cell death as an alternative to autophagy. Strikingly, antioxidant treatment prevented UPR activation and autophagy while restoring the proliferative capacity of these cells. Our results indicate that ROS are a critical signal generated by disruption of the P complex that causes a cellular response that follows a sequential order: first ROS, then ER stress/UPR activation, and finally autophagy. Importantly, inhibition of the first step alone is able to restore the proliferative capacity of the cells, preventing UPR activation and autophagy. Overall, our results support a role for autophagy as a survival mechanism in response to stress due to RPLP protein deficiency.
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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.