ArticleNucleic acids research2016
Cancer-predisposition gene KLLN maintains pericentric H3K9 trimethylation protecting genomic stability.
Article in Nucleic acids research, 2016. 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, 17 citations in OpenAlex.
- Epigenetic control of telomeric RNA maintains heterochromatin in telomerase-driven cancers.Signal transduction and targeted therapy · 2026Article
- Micronuclei: origins, assays, mechanisms, diseases and treatments.Signal transduction and targeted therapy · 2026Review
- Source, co-occurrence, and prognostic value of PTEN mutations or loss in colorectal cancer.NPJ genomic medicine · 2023Article
- Mechanistic insights into the dual role of CCAR2/DBC1 in cancer.Experimental & molecular medicine · 2023Review
- p53-mediated G1 arrest requires the induction of both p21 and Killin in human colon cancer cells.Cell cycle (Georgetown, Tex.) · 2022Article
- Identification of nuclear export signal in KLLN suggests potential role in proteasomal degradation in cancer cells.Oncotarget · 2020Article
- PTEN hamartoma tumour syndrome: what happens when there is no PTEN germline mutation?Human molecular genetics · 2020Review
- H3K9me3 maintenance on a human artificial chromosome is required for segregation but not centromere epigenetic memory.Journal of cell science · 2020Article
- SUV39H1 regulates human colon carcinoma apoptosis and cell cycle to promote tumor growth.Cancer letters · 2020Article
- SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion.Cancer immunology research · 2019Article
- Non-canonical role of cancer-associated mutant SEC23B in the ribosome biogenesis pathway.Human molecular genetics · 2018Article
- KLLN-mediated DNA damage-induced apoptosis is associated with regulation of p53 phosphorylation and acetylation in breast cancer cells.Cell death discovery · 2018Article
- Calcium depletion destabilises kinetochore fibres by the removal of CENP-F from the kinetochore.Scientific reports · 2017Article
- Heterochromatin Reduction Correlates with the Increase of the KDM4B and KDM6A Demethylases and the Expression of Pericentromeric DNA during the Acquisition of a Transformed Phenotype.Journal of Cancer · 2017Article
- Histone 3.3 hotspot mutations in conventional osteosarcomas: a comprehensive clinical and molecular characterization of six H3F3A mutated cases.Clinical sarcoma research · 2017Article
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 3 institutions in 1 country.
Funding
Abstract
Maintenance of proper chromatin states and genomic stability is vital for normal development and health across a range of organisms. Here, we report on the role of KLLN in maintenance of pericentric H3K9 trimethylation (H3K9me3) and genomic stability. Germline hypermethylation of KLLN, a gene uncovered well after the human genome project, has been linked to Cowden cancer-predisposition syndrome (CS) in PTEN wild-type cases. KLLN first identified as a p53-dependent tumor suppressor gene, was believed to bind randomly to DNA and cause S-phase arrest. Using chromatin immunoprecipitation-based sequencing (ChIP-seq), we demonstrated that KLLN binds to DNA regions enriched with H3K9me3. KLLN overexpression correlated with increased H3K9 methyltransferase activity and increased global H3K9me3, while knockdown of KLLN had an opposite effect. We also found KLLN to localize to pericentric regions, with loss of KLLN resulting in dysregulation of pericentric heterochromatin, with consequent chromosomal instability manifested by increased micronuclei formation and numerical chromosomal aberrations. Interestingly, we show that KLLN interacts with DBC1, with consequent abrogation of DBC1 inhibition of SUV39H1, a H3K9 methyltransferase, suggesting the mode of KLLN regulating H3K9me3. These results suggest a critical role for KLLN as a potential regulator of pericentric heterochromatin formation, genomic stability and gene expression.
Indexed as
Identifiers
What OpenQuestion holds
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.