<scp>lncRNA</scp>: A new danger for genome integrity

Шмакова, А. А.; Vassetzky, Yegor S.

doi:10.1002/ijc.34397

Cited by 1 publication

(2 citation statements)

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“…due to chromatin state or the activity of intrinsic DNA-cutting enzymes ( 9 , 11 )] and/or predetermined factors that affect DNA repair [e.g. transcriptional activity, loci spatial proximity, the activity of specific repair factors or even cell-specific expression of chromosomal aberrations stimulating long noncoding RNAs (lncRNAs) ( 12 )]. While previous studies have extensively explored the occurrence of cell-specific DSBs, less is known about the risk factors that interfere with translocation-prone DSB repair once they are already formed in a particular cell type.…”

Section: Introductionmentioning

confidence: 99%

“…The presence of specific transcripts [e.g. lncRNAs that share homology regions for two different loci ( 12 , 13 )] or certain drugs ( 14 ) can also affect the formation of chromosomal rearrangements. Understanding these risk factors is crucial for developing targeted interventions to prevent the occurrence of translocations and the development of related diseases such as cancer.…”

Section: Introductionmentioning

confidence: 99%

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Specificity of cancer-related chromosomal translocations is linked to proximity after the DNA double-strand break and subsequent selection

Canoy,

Shmakova,

Karpukhina

et al. 2023

NAR Cancer

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Most cancer-related chromosomal translocations appear to be cell type specific. It is currently unknown why different chromosomal translocations occur in different cells. This can be due to either the occurrence of particular translocations in specific cell types or adaptive survival advantage conferred by translocations only in specific cells. We experimentally addressed this question by double-strand break (DSB) induction at MYC, IGH, AML and ETO loci in the same cell to generate chromosomal translocations in different cell lineages. Our results show that any translocation can potentially arise in any cell type. We have analyzed different factors that could affect the frequency of the translocations, and only the spatial proximity between gene loci after the DSB induction correlated with the resulting translocation frequency, supporting the ‘breakage-first’ model. Furthermore, upon long-term culture of cells with the generated chromosomal translocations, only oncogenic MYC–IGH and AML–ETO translocations persisted over a 60-day period. Overall, the results suggest that chromosomal translocation can be generated after DSB induction in any type of cell, but whether the cell with the translocation would persist in a cell population depends on the cell type-specific selective survival advantage that the chromosomal translocation confers to the cell.

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Section: Introductionmentioning

confidence: 99%