ArticleEpigenetics & chromatin2019
DNA methylation modifier LSH inhibits p53 ubiquitination and transactivates p53 to promote lipid metabolism.
Article in Epigenetics & chromatin, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 54 citations in OpenAlex.
- YOD1 promotes ferroptosis in acute lung injury by deubiquitination of NCOA4.Communications biology · 2025Article
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- Deubiquitylase YOD1 regulates CDK1 stability and drives triple-negative breast cancer tumorigenesis.Journal of experimental & clinical cancer research : CR · 2023Article
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- Signaling pathways in cancer metabolism: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- GPR162 activates STING dependent DNA damage pathway as a novel tumor suppressor and radiation sensitizer.Signal transduction and targeted therapy · 2023Article
- Association between abnormal lipid metabolism and tumor.Frontiers in endocrinology · 2023Review
- The chromatin remodelling protein LSH/HELLS regulates the amount and distribution of DNA hydroxymethylation in the genome.Epigenetics · 2022Article
- Lymphoid-specific helicase in epigenetics, DNA repair and cancer.British journal of cancer · 2022Review
- HELLS Is Negatively Regulated by Wild-Type P53 in Liver Cancer by a Mechanism Involving P21 and FOXM1.Cancers · 2022Article
- Diagnostic, Prognostic, and Immunological Roles of HELLS in Pan-Cancer: A Bioinformatics Analysis.Frontiers in immunology · 2022Article
- The Organelle-Specific Regulations and Epigenetic Regulators in Ferroptosis.Frontiers in pharmacology · 2022Review
- Proline dehydrogenase in cancer: apoptosis, autophagy, nutrient dependency and cancer therapy.Amino acids · 2021Review
- The role of ferroptosis in lung cancer.Biomarker research · 2021Review
- A Nuclear Long Non-Coding RNA LINC00618 Accelerates Ferroptosis in a Manner Dependent upon Apoptosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Regulating tumor suppressor genes: post-translational modifications.Signal transduction and targeted therapy · 2020Review
- High Glucose Induces Lipid Accumulation via 25-Hydroxycholesterol DNA-CpG Methylation.iScience · 2020Article
- Article
- The epigenetic regulators and metabolic changes in ferroptosis-associated cancer progression.Molecular cancer · 2020Review
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe stability of p53 is mainly controlled by ubiquitin-dependent degradation, which is triggered by the E3 ubiquitin ligase MDM2. The chromatin modifier lymphoid-specific helicase (LSH) is essential for DNA methylation and cancer progression as a transcriptional repressor. The potential interplay between chromatin modifiers and transcription factors remains largely unknown.
resultsHere, we present data suggesting that LSH regulates p53 in cis through two pathways: prevention proteasomal degradation through its deubiquitination, which is achieved by reducing the lysine 11-linked, lysine 48-linked polyubiquitin chains (K11 and K48) on p53; and revival of the transcriptional activity of p53 by forming a complex with PKM2 (pyruvate kinase 2). Furthermore, we confirmed that the LSH-PKM2 interaction occurred at the intersubunit interface region of the PKM2 C-terminal region and the coiled-coil domains (CC) and ATP-binding domains of LSH, and this interaction regulated p53-mediated transactivation in cis in lipid metabolism, especially lipid catabolism.
conclusionThese findings suggest that LSH is a novel regulator of p53 through the proteasomal pathway, thereby providing an alternative mechanism of p53 involvement in lipid metabolism in cancer.
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