ArticleOncogenesis2020
Chromatin remodeling protein HELLS is critical for retinoblastoma tumor initiation and progression.
Article in Oncogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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
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Who cites it
29 citing papers in PubMed, 37 citations in OpenAlex.
- Epigenetic Factor Dysregulation and Distinct Expression Signatures in Retinoblastoma: A Transcriptomic Analysis.Investigative ophthalmology & visual science · 2026Article
- Dysregulated HELLS expression alters cellular processes and serves as a potential prognostic marker in acute myeloid leukemia.The Journal of biological chemistry · 2026Article
- Photoclick chemistry led to the identification of HELLS as a helicase for DNA G-quadruplexes.Nucleic acids research · 2026Article
- HELLS Knockdown Inhibits the Malignant Progression of Lung Adenocarcinoma Via Blocking Akt/CREB Pathway by Downregulating KIF11.Molecular biotechnology · 2025Article
- MiR-335-5p Escaped from CircKIAA0586 Adsorption Contributes to Mechanical Overloading-Induced Cartilage Degeneration by Targeting Lymphoid-Specific Helicase.Research (Washington, D.C.) · 2025Article
- DNA methylation regulates B cell activation via repressing Pax5 expression in teleost.Frontiers in immunology · 2024Article
- Identification of the ferroptosis regulator HELLS with prognostic value for adrenocortical carcinoma based on integrated analysis and experimental validation.Gland surgery · 2023Article
- Genetics in ophthalmology: molecular blueprints of retinoblastoma.Human genomics · 2023Review
- Retinoblastoma: A review of the molecular basis of tumor development and its clinical correlation in shaping future targeted treatment strategies.Indian journal of ophthalmology · 2023Review
- Combined inhibition of histone deacetylase and cytidine deaminase improves epigenetic potency of decitabine in colorectal adenocarcinomas.Clinical epigenetics · 2023Article
- CRdb: a comprehensive resource for deciphering chromatin regulators in human.Nucleic acids research · 2023Article
- Immunological function and prognostic value of lymphoid-specific helicase in liver hepatocellular carcinoma.Cancer biomarkers : section A of Disease markers · 2023Article
- Ferroptosis-related genes in cervical cancer as biomarkers for predicting the prognosis of gynecological tumors.Frontiers in molecular biosciences · 2023Article
- UHRF1 overexpression promotes osteosarcoma metastasis through altered exosome production and AMPK/SEMA3E suppression.Oncogenesis · 2022Article
- The Chromatin Remodeler HELLS: A New Regulator in DNA Repair, Genome Maintenance, and Cancer.International journal of molecular sciences · 2022Review
- Signal pathways and precision therapy of small-cell lung cancer.Signal transduction and targeted therapy · 2022Review
- Genome maintenance in retinoblastoma: Implications for therapeutic vulnerabilities.Oncology letters · 2022Review
- Lymphoid-specific helicase in epigenetics, DNA repair and cancer.British journal of cancer · 2022Review
- Hsa_circ_0046523 Mediates an Immunosuppressive Tumor Microenvironment by Regulating MiR-148a-3p/PD-L1 Axis in Pancreatic Cancer.Frontiers in oncology · 2022Article
- In Silico Analysis to Explore Lineage-Independent and -Dependent Transcriptional Programs Associated with the Process of Endothelial and Neural Differentiation of Human Induced Pluripotent Stem Cells.Journal of clinical medicine · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Retinoblastoma is an aggressive childhood cancer of the developing retina that initiates by biallelic RB1 gene inactivation. Tumor progression in retinoblastoma is driven by epigenetics, as retinoblastoma genomes are stable, but the mechanism(s) that drive these epigenetic changes remain unknown. Lymphoid-specific helicase (HELLS) protein is an epigenetic modifier directly regulated by the RB/E2F pathway. In this study, we used novel genetically engineered mouse models to investigate the role of HELLS during retinal development and tumorigenesis. Our results indicate that Hells-null retinal progenitor cells divide, undergo cell-fate specification, and give rise to fully laminated retinae with minor bipolar cells defects, but normal retinal function. Despite the apparent nonessential role of HELLS in retinal development, failure to transcriptionally repress Hells during retinal terminal differentiation due to retinoblastoma (RB) family loss significantly contributes to retinal tumorigenesis. Loss of HELLS drastically reduced ectopic division of differentiating cells in Rb1/p107-null retinae, significantly decreased the incidence of retinoblastoma, delayed tumor progression, and increased overall survival. Despite its role in heterochromatin formation, we found no evidence that Hells loss directly affected chromatin accessibility in the retina but functioned as transcriptional co-activator of E2F3, decreasing expression of cell cycle genes. We propose that HELLS is a critical downstream mediator of E2F-dependent ectopic proliferation in RB-null retinae. Together with the nontoxic effect of HELLS loss in the developing retina, our results suggest that HELLS and its downstream pathways could serve as potential therapeutic targets for retinoblastoma.
Identifiers
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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.