ArticleCancer research2016
Chromatin Remodeling Factor LSH Drives Cancer Progression by Suppressing the Activity of Fumarate Hydratase.
Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 100 citations in OpenAlex.
- Evaluation of the subtype-specific epigenetic prognostic association of HELLS in non-small cell lung cancer: integrated clinical and molecular insights.Translational cancer research · 2026Article
- Dysregulated HELLS expression alters cellular processes and serves as a potential prognostic marker in acute myeloid leukemia.The Journal of biological chemistry · 2026Article
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
- HELLS inhibits autophagy‑dependent ferroptosis in nasopharyngeal carcinoma by modulating the Nrf2/HO‑1/GPX4 pathway.International journal of molecular medicine · 2026Article
- Dual roles of USP1 in HELLS deubiquitination and SUMOylation drive EMT and FOLFOX-based chemoresistance.Oncogenesis · 2025Article
- Integrated machine learning and single-cell analysis identify chromatin-remodeling gene signature for diagnosis and prognosis in nasopharyngeal carcinoma.Clinical and experimental medicine · 2025Article
- Transcending frontiers in prostate cancer: the role of oncometabolites on epigenetic regulation, CSCs, and tumor microenvironment to identify new therapeutic strategies.Cell communication and signaling : CCS · 2024Review
- The Tricarboxylic Acid Cycle Metabolites for Cancer: Friend or Enemy.Research (Washington, D.C.) · 2024Review
- The Role of TGFBR3 in the Development of Lung Cancer.Protein and peptide letters · 2024Review
- ΔNp63α-mediated epigenetic regulation in keratinocyte senescence.Epigenetics · 2023Article
- Fumarate hydratase (FH) and cancer: a paradigm of oncometabolism.British journal of cancer · 2023Review
- Article
- The PLOD2/succinate axis regulates the epithelial-mesenchymal plasticity and cancer cell stemness.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- GPR162 activates STING dependent DNA damage pathway as a novel tumor suppressor and radiation sensitizer.Signal transduction and targeted therapy · 2023Article
- Ferroptosis-related genes in cervical cancer as biomarkers for predicting the prognosis of gynecological tumors.Frontiers in molecular biosciences · 2023Article
- The Chromatin Remodeler HELLS: A New Regulator in DNA Repair, Genome Maintenance, and Cancer.International journal of molecular sciences · 2022Review
- Epigenetic editing and tumor-dependent immunosuppressive signaling in head and neck malignancies.Oncology letters · 2022Review
- miRNA-guided reprogramming of glucose and glutamine metabolism and its impact on cell adhesion/migration during solid tumor progression.Cellular and molecular life sciences : CMLS · 2022Review
- Lymphoid-specific helicase in epigenetics, DNA repair and cancer.British journal of cancer · 2022Review
- The Epithelial-Mesenchymal Transition at the Crossroads between Metabolism and Tumor Progression.International journal of molecular sciences · 2022Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
22 authors at 4 institutions in 3 countries.
Funding
Abstract
Chromatin modification is pivotal to the epithelial-mesenchymal transition (EMT), which confers potent metastatic potential to cancer cells. Here, we report a role for the chromatin remodeling factor lymphoid-specific helicase (LSH) in nasopharyngeal carcinoma (NPC), a prevalent cancer in China. LSH expression was increased in NPC, where it was controlled by the Epstein-Barr virus-encoded protein LMP1. In NPC cells in vitro and in vivo, LSH promoted cancer progression in part by regulating expression of fumarate hydratase (FH), a core component of the tricarboxylic acid cycle. LSH bound to the FH promoter, recruiting the epigenetic silencer factor G9a to repress FH transcription. Clinically, we found that the concentration of TCA intermediates in NPC patient sera was deregulated in the presence of LSH. RNAi-mediated silencing of FH mimicked LSH overexpression, establishing FH as downstream mediator of LSH effects. The TCA intermediates α-KG and citrate potentiated the malignant character of NPC cells, in part by altering IKKα-dependent EMT gene expression. In this manner, LSH furthered malignant progression of NPC by modifying cancer cell metabolism to support EMT. Cancer Res; 76(19); 5743-55. ©2016 AACR.
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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.