A simpler twist of fate

Eisenstein, Michael

doi:10.1038/534421a

Cited by 2 publications

(2 citation statements)

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“…Scientific discoveries keep highlighting and clarifying the mechanisms controlling cell proliferation and differentiation. While the four transcription factors of the Yamanaka cocktail have been shown to be sufficient to induce pluripotency (1), further research has focused on the mechanisms of stem cell differentiation, their plasticity and trans-differentiation potential (2). Investigations of the reprogramming of cancer cells, which possess characteristics similar to those of stem cells, is a main topic in cancer research (3).…”

Section: Introductionmentioning

confidence: 99%

“…Through their ability to regulate gene expression, ZNF proteins are involved in cell proliferation, differentiation and cancer progression (4, 5). The C(2)H(2) zinc fingers (6), CCCH zinc fingers (7) and the RanBP2 type zinc fingers (8) may be involved in RNA binding promoting regulation of mRNA expression or processing. Depending on the presence of protein-binding domains, such as BTB/POZ, Krüppel-associated box (KRAB) and SCAN, ZNF may be involved in protein-protein interaction (5).…”

Section: Introductionmentioning

confidence: 99%

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DiPRO1 dependent transcriptional and epigenetic regulation distinctly controls the fate of muscle and mesenchymal cancer cells

Rich

Bennaroch

Notel

et al. 2023

Preprint

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We have recently identified the uncharacterized ZNF555 protein as a component of a productive complex, which is involved in the morbid function of the 4qA locus in facioscapulohumeral dystrophy. As a result of our current findings, ZNF555 is hereinafter referred to as DiPRO1 (Death, Differentiation and PROliferation related PROtein 1). In this study, we provide substantial evidence that DiPRO1 plays a role in human myoblast differentiation. It acts on regulatory binding regions of SIX1, which is a master regulator of myogenesis. We further describe the relevance of DiPRO1 in mesenchymal tumors, such as rhabdomyosarcoma (RMS) and Ewing sarcoma. DiPRO1 plays a repressor role in these tumors via the epigenetic regulators TIF1B and UHRF1 in order to maintain methylation of regulatory cis-elements and promoters. Loss of DiPRO1 eradicates cancer cells, by switching on a distinct transcriptional and epigenetic program. It consists of mimicking the host defense against the virus response by awakening the retrotransposable repeats (RE) and the ZNP/KZFP gene family. DiPRO1 also contributes to the balance of cellular decisions toward inflammation and/or apoptosis by controlling TNF-α via NF-kappaB signaling. Finally, we demonstrate that mesenchymal cancer tumors are vulnerable in response to si/shDiPRO1-based nanomedicines, positioning DiPRO1 as a potential new target for therapeutic intervention.

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Section: Introductionmentioning

confidence: 99%