ArticleCell cycle (Georgetown, Tex.)2015
Sestrin2 facilitates death receptor-induced apoptosis in lung adenocarcinoma cells through regulation of XIAP degradation.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- SREBF1-mediated SND1 transcriptional activation promotes prostate cancer progression via MTDH interaction through the SESN2/AMPK/mTOR axis.Journal of translational medicine · 2025Article
- Article
- Review
- p53-regulated SESN1 and SESN2 regulate cell proliferation and cell death through control of STAT3.Cell communication and signaling : CCS · 2025Article
- Review
- Antioxidant genes in cancer and metabolic diseases: Focusing on Nrf2, Sestrin, and heme oxygenase 1.International journal of biological sciences · 2024Review
- Sestrin2: multifaceted functions, molecular basis, and its implications in liver diseases.Cell death & disease · 2023Review
- Sestrin2 in cancer: a foe or a friend?Biomarker research · 2022Review
- The functions and roles of sestrins in regulating human diseases.Cellular & molecular biology letters · 2022Review
- RNA Exosome Component EXOSC4 Amplified in Multiple Cancer Types Is Required for the Cancer Cell Survival.International journal of molecular sciences · 2022Article
- A paradoxical role for sestrin 2 protein in tumor suppression and tumorigenesis.Cancer cell international · 2021Review
- Article
- Sestrin2 as a gatekeeper of cellular homeostasis: Physiological effects for the regulation of hypoxia-related diseases.Journal of cellular and molecular medicine · 2021Review
- Sestrins in Physiological Stress Responses.Annual review of physiology · 2021Review
- Sestrins: Darkhorse in the regulation of mitochondrial health and metabolism.Molecular biology reports · 2020Review
- Sestrin2 Expression Has Regulatory Properties and Prognostic Value in Lung Cancer.Journal of personalized medicine · 2020Article
- Mitochondrial localization of SESN2.PloS one · 2020Article
- CC-223, NSC781406, and BGT226 Exerts a Cytotoxic Effect Against Pancreatic Cancer Cells via mTOR Signaling.Frontiers in pharmacology · 2020Article
- p53-inducible SESTRINs might play opposite roles in the regulation of early and late stages of lung carcinogenesis.Oncotarget · 2019Article
- Induction of sestrin 2 is associated with fisetin-mediated apoptosis in human head and neck cancer cell lines.Journal of clinical biochemistry and nutrition · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Apoptosis plays a critical physiological role in controlling cell number and eliminating damaged, non-functional and transformed cells. Cancerous cells as well as some types of normal cells are often resistant to cell death induced by pro-inflammatory cytokines through death receptors. This potentially allows cancer cells to evade the control from the immune system and to proceed toward a more malignant stage, although the mechanisms of this evasion are not well established. We have recently identified the stress-responsive Sestrin2 protein as a critical regulator of cell viability under stress conditions. Sestrin2 is a member of a small family of antioxidant proteins and inhibitors of mechanistic Target of Rapamycin Complex 1 (mTORC1) kinase. Down-regulation of Sestrin1/2 leads to genetic instability and accelerates the growth of lung adenocarcinoma xenografts. Here we addressed the potential role of Sestrin2 in regulation of cell death induced by TNFR1 and related Fas and TRAIL receptors in lung adenocarcinoma cells. We found that Sestrin2 silencing strongly inhibits cytokine-induced cell death through a mechanism independent of ROS and mTORC1 regulation. We determined that the X-linked inhibitor of apoptosis protein (XIAP) plays a critical role in the control of cytokine-induced cell death by Sestrin2. Thus our study defines a new, previously unrecognized role of Sestrin2 in the regulation of apoptosis.
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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.