Histone methylation codes involved in stemness, multipotency, and senescence in budding tunicates

Kawamura, Kaz; Kinoshita, Miyuki; Sekida, Satoko; Sunanaga, Takeshi

doi:10.1016/j.mad.2014.12.001

Cited by 7 publications

(2 citation statements)

References 52 publications

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“…Enrichment of H3K4me3 at promoters of stemness genes OCT4, Nanog and Sox2 were reported during erythroblast erythroid differentiation but completely lost at upon erythroid differentiation 41 . H3K27me3 and H3K4me3 double-positive signals are involved in cell stemness 42 . Therefore, the overexpression of KMT2A and KMT2C could maintain the chromatin active signature and facilitate the maintenance of stemness in cancer stem cells.…”

Section: Discussionmentioning

confidence: 99%

LncRNA OIP5-AS1 is overexpressed in undifferentiated oral tumors and integrated analysis identifies as a downstream effector of stemness-associated transcription factors

Arunkumar

Anand

Raksha

et al. 2018

Sci Rep

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Long non-coding RNAs (lncRNAs) play an important role in the regulation of key cellular processes in early development and cancer. LncRNA Oip5-as1 facilitates stem cell self-renewal in mouse by sponging mmu-miR-7 and modulating NANOG level, yet its role in cancer is less understood. We analyzed OIP5-AS1 expression in oral tumors and in TCGA datasets. We observed overexpression of OIP5-AS1 in oral tumors (P < 0.001) and in tumors of epithelial origin from TCGA. OIP5-AS1 expression was strongly associated with undifferentiated tumors (P = 0.0038). In silico analysis showed miR-7 binding site is conserved in mouse and human OIP5-AS1. However, human NANOG 3′-UTR lost the binding site for hsa-miR-7a-3. Therefore, we screened for other miRNAs that can be sponged by OIP5-AS1 and identified six potential miRNAs and their downstream target genes. Expression analysis showed downregulation of miRNAs and upregulation of downstream target genes, particularly in undifferentiated tumors with high-level of OIP5-AS1 suggesting OIP5-AS1 could post-transcriptionally modulate the downstream target genes. Further, systematic epigenomic analysis of OIP5-AS1 promoter revealed binding motifs for MYC, NANOG and KLF4 suggesting that OIP5-AS1 could be transactivated by stemness-associated transcription factors in cancer. OIP5-AS1 overexpression in undifferentiated oral tumors may be suggestive of enhanced cancer stemness, and consequently, poor clinical outcome.

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Section: Discussionmentioning

confidence: 99%

LncRNA OIP5-AS1 is overexpressed in undifferentiated oral tumors and integrated analysis identifies as a downstream effector of stemness-associated transcription factors

Arunkumar

Anand

Raksha

et al. 2018

Sci Rep

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“…Several recent studies have reported that epigenetic changes play an important role in some cardiovascular pathologies (Han et al, 2015) and regulation of the aging process (Brunet and Berger, 2014). Histone methylation is one of the epigenetic modifications that occurs as a hallmark of aging (McCauley and Dang, 2014;Kawamura et al, 2015). Age-related changes in histone methylation were reported in Drosophila (Wood et al, 2010), mouse brain (Wang et al, 2010), and rat kidney and liver (Sarg et al, 2002).…”

Section: Femalementioning

confidence: 99%

Age- and sex-dependent alteration of functions and epigenetic modifications of vessel and endothelium related biomarkers

Han¹,

Aydın²,

Akansel³

et al. 2018

Turk J Biol

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Introduction Aging is a natural process for every living organism. The trouble here is increased health problems as a result of aging. Aging is a dominant risk factor for cardiovascular diseases and is associated with progressive vascular dysfunction (Herrera et al., 2010; Laurent, 2012). Many studies reported a sex difference in age-associated vascular changes (Sarabi et al., 1999; Sader and Celermajer, 2002; Okumura et al., 2011). Celermajer et al. (1994) showed that age-related impairment in endothelial function appeared to occur earlier in males than in females. Different regulation of endothelial function is one of the main mechanisms underlying the variation in age-associated vascular changes in females and males (Sarabi et al., 1999). However, the underlying mechanisms of sex-dependent alterations in endothelial function remain to be investigated. Endothelium-derived NO plays a key role in the regulation of vascular homeostasis (Moncada et al., 1991). The capacity of NO release is considered to be a major indicator of endothelial function. Vascular aging characterized by endothelial dysfunction is associated with reduced NO bioavailability and increased generation of reactive oxygen species (ROS). ROS combine with NO and produce deleterious free radicals, leading to endothelial dysfunction (Heitzer et al., 2001; Tsimakis, 2006; El Assar et al., 2013; Rochette et al., 2013). ADMA is an endogenous competitive inhibitor of NO synthase and an increase in ADMA is associated with impairment of NO synthesis (Bouras et al., 2013; Sverdlov et al., 2014). It has been reported that plasma concentrations of ADMA increase in elderly people and in postmenopausal women (Schulze et al., 2005). H 2 S is acknowledged as an important gaseous signaling molecule (Kolluru et al., 2013). It has been revealed that H 2 S is an endogenous regulator of oxidative damage and aging in C. elegans (Qabazard et al., 2014). However, the relationship between these molecules and endothelial function in the aging process is still largely unknown. Recent studies have focused on epigenetic changes that occur as a hallmark of aging (Brunet and Berger, 2014).

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Stat stimulates histone H3K4 methylation via KDM5 inhibition in adult stem cells of budding tunicates

Kimura‐Nagano,

Kishimoto,

Sekida

et al. 2024

Developmental Dynamics

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BackgroundThe branchial epithelium is one of the main tissues in which histone H3K4 trimethylation (H3K4me3) occurs in the budding tunicate, Polyandrocarpa misakiensis. It contains proliferating and undifferentiated cell aggregates at the bottom of each pharyngeal cleft, providing the nest for the adult stem cell niche. We examined the sustainable mechanism enabling epigenetic histone methylation in adult stem cells.ResultsHistone H3K4 demethylase (PmisKdm5) was not co‐expressed in vivo with the transcription factor, signal transduction and activator of transcription (PmisStat) in the same cells. PmisStat mRNA, when electroporated into zooids, suppressed the gene expression of PmisKdm5 and facilitated the trimethylation of H3K4. A STAT5 inhibitor blocked the nuclear localization of PmisStat. It stimulated PmisKdm5 gene expression irrespective of PmisStat mRNA. The KDM5 inhibitor, CPI‐455, stimulated H3K4me3 similarly to PmisStat mRNA. PmisStat mRNA and CPI‐455 both induced the gene expression of PmisAp2 and PmisSp8, which were recently identified as budding/regeneration‐related genes. When zooid tissues were treated with both CPI‐455 and the STAT5 inhibitor, CPI‐455 overwhelmed the effects of the STAT inhibitor on PmisAp2 and PmisSp8.ConclusionPmisStat is involved in epigenetic histone methylation at H3K4 through the inhibition of PmisKdm5. H3K4me3 affects downstream gene expression more directly and strongly than PmisStat.

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Histone methylation codes involved in stemness, multipotency, and senescence in budding tunicates

Cited by 7 publications

References 52 publications

LncRNA OIP5-AS1 is overexpressed in undifferentiated oral tumors and integrated analysis identifies as a downstream effector of stemness-associated transcription factors

LncRNA OIP5-AS1 is overexpressed in undifferentiated oral tumors and integrated analysis identifies as a downstream effector of stemness-associated transcription factors

Age- and sex-dependent alteration of functions and epigenetic modifications of vessel and endothelium related biomarkers

Stat stimulates histone H3K4 methylation via KDM5 inhibition in adult stem cells of budding tunicates

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