ArticleNature communications2023
p53 restoration in small cell lung cancer identifies a latent cyclophilin-dependent necrosis mechanism.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- Exploring the sex-dependent effects of midnolin loss on hepatic transcription and chromatin accessibility.Biochemistry and biophysics reports · 2026Article
- ALOX12 suppresses colon cancer progression by promoting p53-mediated ferroptosis through upregulating ROS-induced stress.Translational cancer research · 2026Article
- Infrequent HPV Infection in Colorectal Neuroendocrine Carcinoma: Molecular and Histologic Characteristics.Diagnostics (Basel, Switzerland) · 2025Article
- Bio-engineered microRNA-7 effectively interferes with the Akt3/p53 axis to suppress human non-small cell lung cancer.Cancer cell international · 2025Article
- Identification of Key Genes Related to Intramuscular Fat Content of Psoas Major Muscle in Saba Pigs by Integrating Bioinformatics and Machine Learning Based on Transcriptome Data.Animals : an open access journal from MDPI · 2025Article
- Current and future therapies for small cell lung carcinoma.Journal of hematology & oncology · 2025Review
- Review
- Review
- Enhanced Lung Cancer Detection Using a Combined Ratio of Antigen-Autoantibody Immune Complexes against CYFRA 21-1 and p53.Cancers · 2024Article
- PPIL1 Drives Hepatocellular Carcinoma Progression and Cancer Stem Cell Self-renewal Through DAAM2-mediated Wnt/β-Catenin Activation.Cancer genomics & proteomicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
The p53 tumor suppressor regulates multiple context-dependent tumor suppressive programs. Although p53 is mutated in ~90% of small cell lung cancer (SCLC) tumors, how p53 mediates tumor suppression in this context is unknown. Here, using a mouse model of SCLC in which endogenous p53 expression can be conditionally and temporally regulated, we show that SCLC tumors maintain a requirement for p53 inactivation. However, we identify tumor subtype heterogeneity between SCLC tumors such that p53 reactivation induces senescence in a subset of tumors, while in others, p53 induces necrosis. We pinpoint cyclophilins as critical determinants of a p53-induced transcriptional program that is specific to SCLC tumors and cell lines poised to undergo p53-mediated necrosis. Importantly, inhibition of cyclophilin isomerase activity, or genetic ablation of specific cyclophilin genes, suppresses p53-mediated necrosis by limiting p53 transcriptional output without impacting p53 chromatin binding. Our study demonstrates that intertumoral heterogeneity in SCLC influences the biological response to p53 restoration, describes a cyclophilin-dependent mechanism of p53-regulated cell death, and uncovers putative mechanisms for the treatment of this most-recalcitrant tumor type.
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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.