To Grow, Stop or Die? – Novel Tumor-Suppressive Mechanism Regulated by the Transcription Factor E2F

Ozono, Eiko; Shoji, Yasuhiro; Ohtani, Kiyoshi

doi:10.5772/54510

Cited by 4 publications

(5 citation statements)

References 96 publications

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“…During quiescence, unphosphorylated Rb proteins control cell proliferation by binding and inhibiting E2F transcription factors, thus blocking cell cycle progression. During cell growth, signaling pathways that phosphorylate Rb proteins are activated, promoting its disassociation from E2F and allowing for the expression of E2F-dependent genes necessary for cell division [107,108]. Inhibition of p53 and inactivation of Rb by viral oncogenes have been shown to extend the life span of several cell types in culture, but telomeres maintenance is also needed for preventing replicative senescence [106].…”

Section: Immortalizing Human Adult Mscsmentioning

confidence: 99%

Usefulness of Mesenchymal Cell Lines for Bone and Cartilage Regeneration Research

Piñeiro-Ramil

Sanjurjo‐Rodríguez

Castro-Viñuelas

et al. 2019

IJMS

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The unavailability of sufficient numbers of human primary cells is a major roadblock for in vitro repair of bone and/or cartilage, and for performing disease modelling experiments. Immortalized mesenchymal stromal cells (iMSCs) may be employed as a research tool for avoiding these problems. The purpose of this review was to revise the available literature on the characteristics of the iMSC lines, paying special attention to the maintenance of the phenotype of the primary cells from which they were derived, and whether they are effectively useful for in vitro disease modeling and cell therapy purposes. This review was performed by searching on Web of Science, Scopus, and PubMed databases from 1 January 2015 to 30 September 2019. The keywords used were ALL = (mesenchymal AND ("cell line" OR immortal*) AND (cartilage OR chondrogenesis OR bone OR osteogenesis) AND human). Only original research studies in which a human iMSC line was employed for osteogenesis or chondrogenesis experiments were included. After describing the success of the immortalization protocol, we focused on the iMSCs maintenance of the parental phenotype and multipotency. According to the literature revised, it seems that the maintenance of these characteristics is not guaranteed by immortalization, and that careful selection and validation of clones with particular characteristics is necessary for taking advantage of the full potential of iMSC to be employed in bone and cartilage-related research.

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Section: Immortalizing Human Adult Mscsmentioning

confidence: 99%

Usefulness of Mesenchymal Cell Lines for Bone and Cartilage Regeneration Research

Piñeiro-Ramil

Sanjurjo‐Rodríguez

Castro-Viñuelas

et al. 2019

IJMS

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“…Considering the role of these 12 genes in cancer, we briefly suggest possible mechanisms affecting the prognosis of GBM as follows ( 1 ). E2F2 is known as the center of the balance between cell proliferation and apoptosis ( 14 ). As shown in Figure 3C of our study, E2F2 was negatively correlated with all 10 significant genes in subcluster 2-4 (except for PAK1 and MDM2).…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, we hypothesized that E2F2 may be a control tower regulating tumor aggressiveness in GBM. However, the activation of deregulated E2F leading to both growth-promoting pathways or tumor suppressor pathways can result in oncogenic changes ( 14 ). In addition, if the level of free E2F is below the threshold, E2F activates only growth-related target genes.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, if the level of free E2F is below the threshold, E2F activates only growth-related target genes. When the level of E2F exceeds the threshold, E2F activates not only growth-related targets but also pro-apoptotic targets ( 14 , 15 ). Therefore, we hypothesized that E2F2 must be maintained at appropriate levels to properly regulate cell proliferation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…GBM, glioblastoma multiforme; OS, overall survival; PFS, progression-free survival; E2F2, E2F transcription factor 2; CTBP2, C-terminal-binding protein 2; MAFF, MAF bZIP transcription factor F; Nrf2, nuclear factor erythroid 2-related factor 2; ARE, antioxidant response element; SLC2A3, solute carrier family 2 member 3; GLUT3, glucose transporter, type 3; PI3K, phosphatidylinositol 3-kinase; TRAF6, tumor necrosis factor receptor associated factor 6; ECSIT, evolutionarily conserved signaling intermediate in Toll pathways; mROS, mitochondrial reactive oxygen species; HSP90B1, heat shock protein 90 kDa beta member 1; PTN, pleiotrophin; SPARC, secreted protein acidic and cysteine rich; SPARCL1, SPARC like 1; TNFRSF1A, tumor necrosis factor receptor superfamily member 1A; TNF, tumor necrosis factor; IL, interleukin; NF-kB, nuclear factor-kappa B; STAT3, signal transducer and activator of transcription; PAK1, p21 activated kinase 1; AKT, protein kinase B; mTOR, mammalian target of rapamycin; RTK, receptor tyrosine kinase; ID4, inhibitor of DNA binding 4; TGF-b, transforming growth factor beta; DDB2, damage-specific DNA-binding protein 2; MDM2, mouse double minute 2 homolog; DKK3, dickkopf-3. (14,15). Therefore, we hypothesized that E2F2 must be maintained at appropriate levels to properly regulate cell proliferation and apoptosis.…”

Section: Dkk3mentioning

confidence: 99%

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Identification of genes from ten oncogenic pathways associated with mortality and disease progression in glioblastoma

Han

Min²,

Noh³

et al. 2022

Front. Oncol.

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Glioblastoma multiforme (GBM) is the most malignant brain tumor with an extremely poor prognosis. The Cancer Genome Atlas (TCGA) database has been used to confirm the roles played by 10 canonical oncogenic signaling pathways in various cancers. The purpose of this study was to evaluate the expression of genes in these 10 canonical oncogenic signaling pathways, which are significantly related to mortality and disease progression in GBM patients. Clinicopathological information and mRNA expression data of 525 patients with GBM were obtained from TCGA database. Gene sets related to the 10 oncogenic signaling pathways were investigated via Gene Set Enrichment Analysis. Multivariate Cox regression analysis was performed for all the genes significantly associated with mortality and disease progression for each oncogenic signaling pathway in GBM patients. We found 12 independent genes from the 10 oncogenic signaling pathways that were significantly related to mortality and disease progression in GBM patients. Considering the roles of these 12 significant genes in cancer, we suggest possible mechanisms affecting the prognosis of GBM. We also observed that the expression of 6 of the genes significantly associated with a poor prognosis of GBM, showed negative correlations with CD8+ T-cells in GBM tissue. Using a large-scale open database, we identified 12 genes belonging to 10 well-known oncogenic canonical pathways, which were significantly associated with mortality and disease progression in patients with GBM. We believe that our findings will contribute to a better understanding of the mechanisms underlying the pathophysiology of GBM in the future.

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Uncovering Cell Cycle Dysregulations and Associated Mechanisms in Cancer and Neurodegenerative Disorders: A Glimpse of Hope for Repurposed Drugs

Advani,

Kumar

2024

Mol Neurobiol

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To Grow, Stop or Die? – Novel Tumor-Suppressive Mechanism Regulated by the Transcription Factor E2F

Cited by 4 publications

References 96 publications

Usefulness of Mesenchymal Cell Lines for Bone and Cartilage Regeneration Research

Usefulness of Mesenchymal Cell Lines for Bone and Cartilage Regeneration Research

Identification of genes from ten oncogenic pathways associated with mortality and disease progression in glioblastoma

Uncovering Cell Cycle Dysregulations and Associated Mechanisms in Cancer and Neurodegenerative Disorders: A Glimpse of Hope for Repurposed Drugs

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