ArticleOncogenesis2018
RecQL4-Aurora B kinase axis is essential for cellular proliferation, cell cycle progression, and mitotic integrity.
Article in Oncogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- RECQL4 alterations in gliomas and nerve sheath tumors: Expression patterns and therapeutic implications.Journal of neuropathology and experimental neurology · 2025Article
- Review
- RECQ4-MUS81 interaction contributes to telomere maintenance with implications to Rothmund-Thomson syndrome.Nature communications · 2025Article
- Unraveling the mechanisms of RECQL4-mediated cervical cancer progression through the PI3K/AKT pathway.Translational oncology · 2024Article
- Hrq1/RECQL4 regulation is critical for preventing aberrant recombination during DNA intrastrand crosslink repair and is upregulated in breast cancer.PLoS genetics · 2022Article
- Comprehensive analyses unveil novel genomic and immunological characteristics of micropapillary pattern in lung adenocarcinoma.Frontiers in oncology · 2022Article
- Patient-derived iPSCs link elevated mitochondrial respiratory complex I function to osteosarcoma in Rothmund-Thomson syndrome.PLoS genetics · 2021Article
- RNF8 ubiquitinates RecQL4 and promotes its dissociation from DNA double strand breaks.Oncogenesis · 2021Article
- Molecular Mechanisms of the RECQ4 Pathogenic Mutations.Frontiers in molecular biosciences · 2021Review
- A Novel Ruthenium(II) Complex With Lapachol Induces G2/M Phase Arrest Through Aurora-B Kinase Down-Regulation and ROS-Mediated Apoptosis in Human Prostate Adenocarcinoma Cells.Frontiers in oncology · 2021Article
- Prognostic Signature for Lung Adenocarcinoma Patients Based on Cell-Cycle-Related Genes.Frontiers in cell and developmental biology · 2021Article
- Exploration of Prognostic Biomarkers among Replication Factor C Family in the Hepatocellular Carcinoma.Evolutionary bioinformatics online · 2021Article
- Article
- Bioinformatics analysis of BUB1 expression and gene regulation network in lung adenocarcinoma.Translational cancer research · 2020Article
- Interaction between RECQL4 and OGG1 promotes repair of oxidative base lesion 8-oxoG and is regulated by SIRT1 deacetylase.Nucleic acids research · 2020Article
- Organ of Corti size is governed by Yap/Tead-mediated progenitor self-renewal.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Chromosome alignment maintenance requires the MAP RECQL4, mutated in the Rothmund-Thomson syndrome.Life science alliance · 2019Article
- Expression and gene regulation network ofAging · 2019Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human RecQL4 helicase plays critical roles in the maintenance of genomic stability. Mutations in RecQL4 helicase results in three clinically related autosomal recessive disorders: Rothmund-Thomson syndrome (RTS), RAPADILINO, and Baller-Gerold syndrome. In addition to several premature aging features, RTS patients are characterized by aneuploidy involving either loss or gain of a single chromosome. Chromosome mosaicism and isochromosomes involving chromosomes 2, 7, and 8 have been reported in RecQL4-deficient RTS patients, but the precise role of RecQL4 in chromosome segregation/stability remains to be elucidated. Here, we demonstrate that RecQL4 physically and functionally interacts with Aurora B kinase (AURKB) and stabilizes its expression by inhibiting its ubiquitination process. Our study indicates that the N-terminus of RecQL4 interacts with the catalytic domain of AURKB. Strikingly, RecQL4 suppression reduces the expression of AURKB leading to mitotic irregularities and apoptotic cell death. RecQL4 suppression increases the proportion of cells at the G2/M phase followed by an extensive cell death, presumably owing to the accumulation of mitotic irregularities. Both these defects (accumulation of cells at G2/M phase and an improper mitotic exit to sub-G1) are complemented by the ectopic expression of AURKB. Finally, evidence is provided for the requirement of both human telomerase reverse transcriptase and RecQL4 for stable immortalization and longevity of RTS fibroblasts. Collectively, our study suggests that the RecQL4-AURKB axis is essential for cellular proliferation, cell cycle progression, and mitotic stability in human cells.
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.