ArticleOncogene2006
RORA, a large common fragile site gene, is involved in cellular stress response.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 152 citations in OpenAlex.
- Leveraging pleiotropic association using sparse group variable selection in genomics data.BMC medical research methodology · 2022Pooled it
- Genetic variation of clock genes and cancer risk: a field synopsis and meta-analysis.Oncotarget · 2017Pooled it
- Identification of potential susceptibility loci for non-small cell lung cancer through whole genome sequencing in circadian rhythm genes.Scientific reports · 2025Article
- EBV-miR-BART5-5p regulates RORA to promote proliferation and migration of gastric cancer cells.PloS one · 2025Article
- DNMT1-driven methylation of RORA facilitates esophageal squamous cell carcinoma progression under hypoxia through SLC2A3.Journal of translational medicine · 2024Article
- Tumoral periprostatic adipose tissue exovesicles-derived miR-20a-5p regulates prostate cancer cell proliferation and inflammation through the RORA gene.Journal of translational medicine · 2024Article
- Article
- Potential therapeutic targets for age-related macular degeneration: The nuclear option.Progress in retinal and eye research · 2023Review
- ALDOC- and ENO2- driven glucose metabolism sustains 3D tumor spheroids growth regardless of nutrient environmental conditions: a multi-omics analysis.Journal of experimental & clinical cancer research : CR · 2023Article
- Illuminating links between cis-regulators and trans-acting variants in the human prefrontal cortex.Genome medicine · 2022Article
- RORA alleviates LPS-induced apoptosis of renal epithelial cells by promoting PGC-1α transcription.Clinical and experimental nephrology · 2022Article
- The role of retinoid-related orphan receptor-α in cigarette smoke-induced autophagic response.Respiratory research · 2022Article
- Circadian rhythms and cancers: the intrinsic links and therapeutic potentials.Journal of hematology & oncology · 2022Review
- Circadian stabilization loop: the regulatory hub and therapeutic target promoting circadian resilience and physiological health.F1000Research · 2022Review
- RORα Suppresses Cancer-Associated Inflammation by Repressing Respiratory Complex I-Dependent ROS Generation.International journal of molecular sciences · 2021Article
- FANCD2 modulates the mitochondrial stress response to prevent common fragile site instability.Communications biology · 2021Article
- RAR-related orphan receptor A: One gene with multiple functions related to migraine.CNS neuroscience & therapeutics · 2020Article
- Small Molecules Targeting Biological Clock; A Novel Prospective for Anti-Cancer Drugs.Molecules (Basel, Switzerland) · 2020Review
- Melatonin: an endogenous miraculous indolamine, fights against cancer progression.Journal of cancer research and clinical oncology · 2020Review
- Impaired Replication Timing Promotes Tissue-Specific Expression of Common Fragile Sites.Genes · 2020Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Common fragile sites (CFSs) are large genomic regions present in all individuals that are highly unstable and prone to breakage and rearrangement, especially in cancer cells with genomic instability. Eight of the 90 known CFSs have been precisely defined and five of these span genes that extend from 700 kb to over 1.5 Mb of genomic sequence. Although these genes reside within some of the most unstable chromosomal regions in the human genome, they are highly conserved evolutionarily. These genes are targets for large chromosomal deletions and rearrangements in cancer and are frequently inactivated in multiple tumor types. There is also an association between these genes and cellular responses to stress. Based upon the association between large genes and CFSs, we began to systematically test other large genes derived from chromosomal regions that were known to contain a CFS. In this study, we demonstrate that the 730 kb retinoic acid receptor-related orphan receptor alpha (RORA) gene is derived from the middle of the FRA15A (15q22.2) CFS. Although this gene is expressed in normal breast, prostate and ovarian epithelium, it is frequently inactivated in cancers that arise from these organs. RORA was previously shown to be involved in the cellular response to hypoxia and here we demonstrate changes in the amount of RORA message produced in cells exposed to a variety of different cellular stresses. Our results demonstrate that RORA is another very large CFS gene that is inactivated in multiple tumors. In addition, RORA appears to play a critical role in responses to cellular stress, lending further support to the idea that the large CFS genes function as part of a highly conserved stress response network that is uniquely susceptible to genomic instability in cancer cells.
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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.