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A critical role of telomere chromatin compaction in ALT tumor cell growth

ALT tumor cells often contain abundant DNA damage foci at telomeres and rely on the alternative lengthening of telomeres (ALT) mechanism to maintain their telomeres. How the telomere chromatin is regulated and maintained in these cells remains largely unknown. In this study, we present evidence that...

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Detalles Bibliográficos
Autores principales: Shi, Guang, Hu, Yang, Zhu, Xing, Jiang, Yuanling, Pang, Junjie, Wang, Chuanle, Huang, Wenjun, Zhao, Yong, Ma, Wenbin, Liu, Dan, Huang, Junjiu, Songyang, Zhou
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7293046/
https://www.ncbi.nlm.nih.gov/pubmed/32379321
http://dx.doi.org/10.1093/nar/gkaa224
Descripción
Sumario:ALT tumor cells often contain abundant DNA damage foci at telomeres and rely on the alternative lengthening of telomeres (ALT) mechanism to maintain their telomeres. How the telomere chromatin is regulated and maintained in these cells remains largely unknown. In this study, we present evidence that heterochromatin protein 1 binding protein 3 (HP1BP3) can localize to telomeres and is particularly enriched on telomeres in ALT cells. HP1BP3 inhibition led to preferential growth inhibition of ALT cells, which was accompanied by telomere chromatin decompaction, increased presence of C-circles, more pronounced ALT-associated phenotypes and elongated telomeres. Furthermore, HP1BP3 appeared to participate in regulating telomere histone H3K9me3 epigenetic marks. Taken together, our data suggest that HP1BP3 functions on telomeres to maintain telomere chromatin and represents a novel target for inhibiting ALT cancer cells.