ArticleCell communication and signaling : CCS2025
p53-regulated SESN1 and SESN2 regulate cell proliferation and cell death through control of STAT3.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- [Gastrodin alleviates hypobaric hypoxia-induced brain injury in rats by reducing neuronal ferroptosisNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Review
- Pterostilbene attenuates osteoarthritis progression through p53-dependent autophagy activation: evidence from network analysis and experimental validation.Frontiers in pharmacology · 2026Article
- Comprehensive Bioinformatics Analysis and Experimental Verification RNF186 Is a Recurrence Signature Gene of Hepatocellular Carcinoma that Promotes Cell Proliferation.Oncology research · 2026Article
- Extracellular vesicles from long COVID patients promote RUNX2-mediated cellular stress via dysregulated miR-204 and p53 pathway activation.Cell communication and signaling : CCS · 2025Article
- SMAD3 orchestrates RNF167 and STAMBPL1-mediated Sestrin2 ubiquitination to drive gastric cancer progression.Cell division · 2025Article
- Article
- Bioinformatics analysis and preliminary validation of autophagy-related genes in asthma disease.Scientific reports · 2025Article
- Review
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Authors and funding
6 authors.
Funding
Abstract
Sestrin1 and Sestrin2 (SESN1&2) are evolutionarily conserved, stress-responsive proteins that regulate cell growth and viability. The primary target of Sestrins is the mTORC1 protein kinase, an activator of anabolic processes and an autophagy inhibitor. Our previous studies showed that inactivating SESN1&2 in lung adenocarcinoma A549 cells accelerates cell proliferation and confers resistance to cell death without affecting mTORC1 activity, suggesting that SESN1&2 modulate cellular processes via mTORC1-independent mechanisms. This work describes a new mechanism through which SESN1&2 regulate cell proliferation and death by suppressing the STAT3 transcription factor. Normally activated in response to stress and inflammation, STAT3 is frequently overactivated in human cancers. This overactivation promotes the expression of pro-proliferative and anti-apoptotic genes that drive carcinogenesis. We demonstrate that SESN1&2 inactivation stimulates STAT3 by downregulating the PTPRD phosphatase, a protein responsible for STAT3 dephosphorylation. Our study demonstrates that SESN1&2 deficiency may cause STAT3 activation and facilitate carcinogenesis and drug resistance, making SESN1&2 reactivation a potential cancer treatment strategy.
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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.