ReviewBiomarker research2022
Sestrin2 in cancer: a foe or a friend?
Review in Biomarker research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- CDCA4 Promotes Lipid Metabolism in Triple-Negative Breast Cancer Through Activation of the SESN2/mTOR/SREBP1 Pathway.Cancers · 2026Article
- Therapeutic Effects of Zhilong Huoxue Tongyu Capsule on Oxidative Stress and Neuroprotection in a Rat Model of Intracerebral Hemorrhage.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Endoplasmic reticulum stress in disease pathogenesis: its implications for therapy.Signal transduction and targeted therapy · 2026Review
- SESN2 as a Novel Diagnostic and Prognostic Biomarker for Kawasaki Disease and Coronary Artery Lesions.Journal of inflammation research · 2026Article
- Review
- A novel regulatory circuit of ATG4B and SESN3 promotes T cell leukemogenesis.Journal of experimental & clinical cancer research : CR · 2025Article
- A viral Cyclin D homolog protein hijacks the metabolic stress sensor SESN2 to promote primary effusion lymphoma growth.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Reduced serum sestrin 2 levels in Hashimoto's disease: a cross-sectional study on a potential pathophysiological and diagnostic role.Endocrine connections · 2025Article
- Targeting the MDM2-MDM4 interaction interface reveals an otherwise therapeutically active wild-type p53 in colorectal cancer.Molecular oncology · 2025Article
- Investigation of sestrin-2 levels and thiol-disulfide homeostasis in polyp tissue of patients with nasal polyps.Scientific reports · 2025Article
- Endoplasmic reticulum stress in lung cancer.Frontiers in oncology · 2025Review
- Expression of Serum LMAN2 and Sestrin2 in Septic Shock Patients and Exploration of Their Prognostic Value.Journal of inflammation research · 2025Article
- Eugenol alleviates renal ischemia-reperfusion injury induced-endoplasmic reticulum stress via activating Sestrin2.Clinics (Sao Paulo, Brazil) · 2025Article
- The three YTHDF paralogs and VIRMA are strong cross-histotype tumor driver candidates among mNAR cancer · 2024Article
- SESN2 Knockdown Increases Betulinic Acid-Induced Radiosensitivity of Hypoxic Breast Cancer Cells.Cells · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sestrin2 is a conserved antioxidant, metabolism regulator, and downstream of P53. Sestrin2 can suppress oxidative stress and inflammation, thereby preventing the development and progression of cancer. However, Sestrin2 attenuates severe oxidative stress by activating nuclear factor erythroid 2-related factor 2 (Nrf2), thereby enhancing cancer cells survival and chemoresistance. Sestrin2 inhibits endoplasmic reticulum stress and activates autophagy and apoptosis in cancer cells. Attenuation of endoplasmic reticulum stress and augmentation of autophagy hinders cancer development but can either expedite or impede cancer progression under specific conditions. Furthermore, Sestrin2 can vigorously inhibit oncogenic signaling pathways through downregulation of mammalian target of rapamycin complex 1 (mTORC1) and hypoxia-inducible factor 1-alpha (HIF-1α). Conversely, Sestrin2 decreases the cytotoxic activity of T cells and natural killer cells which helps tumor cells immune evasion. Sestrin2 can enhance tumor cells viability in stress conditions such as glucose or glutamine deficiency. Cancer cells can also upregulate Sestrin2 during chemotherapy or radiotherapy to attenuate severe oxidative stress and ER stress, augment autophagy and resist the treatment. Recent studies unveiled that Sestrin2 is involved in the development and progression of several types of human cancer. The effect of Sestrin2 may differ depending on the type of tumor, for instance, several studies revealed that Sestrin2 protects against colorectal cancer, whereas results are controversial regarding lung cancer. Furthermore, Sestrin2 expression correlates with metastasis and survival in several types of human cancer such as colorectal cancer, lung cancer, and hepatocellular carcinoma. Targeted therapy for Sestrin2 or regulation of its expression by new techniques such as non-coding RNAs delivery and vector systems may improve cancer chemotherapy and overcome chemoresistance, metastasis and immune evasion that should be investigated by future trials.
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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 Socratic graph.