English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Lymphoid-specific helicase in epigenetics, DNA repair and cancer

MPS-Authors
/persons/resource/persons239429

Rubio,  Karla
Lung Cancer Epigenetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons224344

Barreto,  Guillermo
Lung Cancer Epigenetics, Max Planck Institute for Heart and Lung Research, Max Planck Society;

External Resource
No external resources are shared
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Chen, X., Li, Y., Rubio, K., Deng, B., Li, Y., Tang, Q., et al. (2021). Lymphoid-specific helicase in epigenetics, DNA repair and cancer. BRITISH JOURNAL OF CANCER. doi:10.1038/s41416-021-01543-2.


Cite as: http://hdl.handle.net/21.11116/0000-0009-4325-2
Abstract
Lymphoid-specific helicase (LSH) is a member of the SNF2 helicase family of chromatin-remodelling proteins. Dysfunctions or mutations in LSH causes an autosomal recessive disease known as immunodeficiency-centromeric instability-facial anomaly (ICF) syndrome. Interestingly, LSH participates in various aspects of epigenetic regulation, including nucleosome remodelling, DNA methylation, histone modifications and heterochromatin formation. Further, LSH plays a crucial role during DNA-damage repair, specifically during double-strand break (DSB) repair, since murine LSH was shown to be essential for non-homologous end joining (NHEJ) and homologous recombination (HR). Accordingly, overexpression of LSH drives tumorigenesis and malignancy. On the other hand, LSH homologs stabilise the genome. Thus, LSH might be implemented as a biomarker for various cancer types and potential target molecule to develop therapeutic strategies against them. In this review, we focus on the role of LSH in orchestrating chromatin rearrangements, such as DNA methylation and histone modifications, as well as in DNA-damage repair. Changes in chromatin structure may facilitate gene expression signatures that cause malignant transformation. We summarise recent findings of LSH in cancers and raise critical open questions for further studies.