Immunohistochemical demonstration of histone H10 in human breast carcinoma

Kostova, Nora; Srebreva, Ljuba; Milev, A.; Bogdanova, Olga G.; Rundquist, Ingemar; Lindner, Herbert; Markov, Dimiter V.

doi:10.1007/s00418-005-0084-y

Cited by 1 publication

(1 citation statement)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The characteristic features of stem cells, including self‐renewal and differentiation ability, mirror the proliferative capacity and the plasticity of cancer cells. Histone H1.0 was shown to be downregulated in a variety of cancers and highly expressed in differentiated normal cells [ 112 ] and a critical role for somatic histone H1.0 in the determination of self‐renewal versus differentiation in cancer stem cells has been demonstrated. [ 113 ] In particular, loss of stochastic repression mediated by histone H1.0 was shown to facilitate destabilization of DNA‐nucleosome interactions, promoting self‐renewal capacity, thus increasing tumorigenic capacity of cancer cells in vivo .…”

Section: Implications For Cancer Biologymentioning

confidence: 99%

Epigenetic regulation of replication origin assembly: A role for histone H1 and chromatin remodeling factors

Falbo

Costanzo

2020

BioEssays

View full text Add to dashboard Cite

During early embryonic development in several metazoans, accurate DNA replication is ensured by high number of replication origins. This guarantees rapid genome duplication coordinated with fast cell divisions. In Xenopus laevis embryos this program switches to one with a lower number of origins at a developmental stage known as mid-blastula transition (MBT) when cell cycle length increases and gene transcription starts. Consistent with this regulation, somatic nuclei replicate poorly when transferred to eggs, suggesting the existence of an epigenetic memory suppressing replication assembly origins at all available sites. Recently, it was shown that histone H1 imposes a non-permissive chromatin configuration preventing replication origin assembly on somatic nuclei. This somatic state can be erased by SSRP1, a subunit of the FACT complex. Here, we further develop the hypothesis that this novel form of epigenetic memory might impact on different areas of vertebrate biology going from nuclear reprogramming to cancer development.

show abstract

Section: Implications For Cancer Biologymentioning

confidence: 99%