Cancer Stem Cell-Inducing Media Activates Senescence Reprogramming in Fibroblasts

Perrigue, Patrick M.; Rakoczy, Magdalena; Pawlicka, Kamila; Belter, Agnieszka; Giel-Pietraszuk, Małgorzata; Naskręt-Barciszewska, Mirosława Z.; Barciszewski, Jan; Figlerowicz, Marek

doi:10.3390/cancers12071745

Cited by 16 publications

(12 citation statements)

References 54 publications

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“…A549 and 293T cells cultured in stem cell medium (SCM) could be converted to cancer stem cells that displayed the phenotype of senescence. Meanwhile, the expression of DNA methyltransferases Dnmt1 and Dnmt3a, histone demethylases Jmjd3 was increased in these cells, which suggested that epigenetic alteration and chromatin remodeling may play a role in cancer stem cell formation and senescence 207 …”

Section: Molecular Mechanisms Of Cancer Stem Cell Senescencementioning

confidence: 95%

Mechanisms of cancer stem cell senescence: Current understanding and future perspectives

Zhang

Monteiro

Liu

et al. 2021

Clin Exp Pharma Physio

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Cancer stem cells (CSCs) are a small population of heterogeneous tumor cells with the capacity of self‐renewal and aberrant differentiation for immortality and divergent lineages of cancer cells. In contrast to bulky tumor cells, CSCs remain less differentiated and resistant to therapy even when targeted with tissue‐specific antigenic markers. This makes CSCs responsible for not only tumor initiation, development, but also tumor recurrence. Emerging evidence suggests that CSCs can undergo cell senescence, a non‐proliferative state of cells in response to stress. While cell senescence attenuates tumor cell proliferation, it is commonly regarded as a tumor suppressive mechanism. However, mounting research indicates that CSC senescence also provides these cells with the capacity to evade cytotoxic effects from cancer therapy, exacerbating cancer relapse and metastasis. Recent studies demonstrate that senescence drives reprogramming of cancer cell toward stemness and promotes CSC generation. In this review, we highlight the origin, heterogeneity and senescence regulatory mechanisms of CSCs, the complex relationship between CSC senescence and tumor therapy, and the recent beneficial effects of senotherapy on eliminating senescent tumor cells.

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Section: Molecular Mechanisms Of Cancer Stem Cell Senescencementioning

confidence: 95%

Mechanisms of cancer stem cell senescence: Current understanding and future perspectives

Zhang

Monteiro

Liu

et al. 2021

Clin Exp Pharma Physio

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“…Inhibition of EZH2 also leads to SASP production via enrichment of H3K27ac, and loss of H3K27me3, at SASP-related loci (Ito et al, 2018). Overexpression of another histone demethylase, UTX, can also silence H3K27me3 to promote cellular senescence (Perrigue et al, 2020).…”

Section: Senescent Cell Characteristicsmentioning

confidence: 99%

Senescence in Wound Repair: Emerging Strategies to Target Chronic Healing Wounds

Wilkinson

Hardman

2020

Front. Cell Dev. Biol.

115

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Cellular senescence is a fundamental stress response that restrains tumour formation. Yet, senescence cells are also present in non-cancerous states, accumulating exponentially with chronological age and contributing to age-and diabetes-related cellular dysfunction. The identification of hypersecretory and phagocytic behaviours in cells that were once believed to be non-functional has led to a recent explosion of senescence research. Here we discuss the profound, and often opposing, roles identified for short-lived vs. chronic tissue senescence. Transiently induced senescence is required for development, regeneration and acute wound repair, while chronic senescence is widely implicated in tissue pathology. We recently demonstrated that sustained senescence contributes to impaired diabetic healing via the CXCR2 receptor, which when blocked promotes repair. Further studies have highlighted the beneficial effects of targeting a range of senescence-linked processes to fight disease. Collectively, these findings hold promise for developing clinically viable strategies to tackle senescence in chronic wounds and other cutaneous pathologies.

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“…Treatment of GC with chrysin, a natural compound frequently present in honey, could significantly upregulate the expression of TET1 and the subsequent elevation of 5-hmC in GC MKN45 cells, thereby inducing cell apoptosis and blocking cell migration/invasion. Thus, the anti-tumor effects of chrysin was mediated through upregulation of TET1 expression in GC, suggesting TET1 as a potentially novel target for GC therapy [119].…”

Section: Natural or Synthetic Small Molecule Compounds Function As Anti-tumor Agents By Upregulation Of Tet1 Expressionmentioning

confidence: 99%

Ten-eleven translocation proteins (TETs): tumor suppressors or tumor enhancers?

Seong

Liu

et al. 2021

Front. Biosci. (Landmark Ed)

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The epigenetic memory stored in the dynamic modifications, such as base modifications of cytosine (C) in DNA, including methylation/hydroxymethylation/demethylation, causes heritable phenotypes via regulating gene expression without alteration of DNA sequence. The process from cytosine modification to the epigenetic effect is orchestrated by complicated machinery consisting of writers, erasers, readers, and other factors. The two major forms of cytosine modification include methylcytosine (5-mC) and hydroxymethylcytosine (5-hmC). DNA methyltransferases (DNMTs) including DNMT1, DNMT3A, and DNMT3B function as writers for 5-mC. The ten-eleven translocation proteins (TET) including TET1, TET2, and TET3 in the mammalian genome are responsible for hydroxymethylation of 5-mC to generate 5-hmC, 5-formylcytosine (5-fC), and 5-carboxylcytosine (5-caC). The 5-mC and 5-hmC have become the two most extensively investigated epigenetic markers, and the dynamic balance of these two markers shape the landscape of the epigenome, functioning as a platform to regulate gene expression epigenetically. The landscape of the 5-hmC in epigenome is precisely and tightly regulated during the development. Aberrant alterations of the epigenetic regulation may cause severe consequences such as phenotype change as well as initiation of disease. Progressively, significant achievements have been made in characterization of writers, erasers, and readers of 5-mC and 5-hmC, as well as the contribution of aberrant alteration of 5-hmC/5-mC landscape to the pathogenesis of human diseases, such as cancers and neurological disorders. This article will highlight the research advances in the distinct contribution of TET proteins as suppressors or promoters to the pathogenesis of tumorigenesis and progression. Furthermore, this article also discusses the challenges and the directions for research in the future.

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Cancer Stem Cell-Inducing Media Activates Senescence Reprogramming in Fibroblasts

Cited by 16 publications

References 54 publications

Mechanisms of cancer stem cell senescence: Current understanding and future perspectives

Mechanisms of cancer stem cell senescence: Current understanding and future perspectives

Senescence in Wound Repair: Emerging Strategies to Target Chronic Healing Wounds

Ten-eleven translocation proteins (TETs): tumor suppressors or tumor enhancers?

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