IGFBP7 Is Not Required for B-RAF-Induced Melanocyte Senescence

Scurr, Lyndee L.; Pupo, Gulietta M.; Becker, Therese M.; Lai, Ken; Schrama, David; Haferkamp, Sebastian; Irvine, Mal; Scolyer, Richard A.; Mann, Graham J.; Becker, Jürgen C.; Kefford, Richard; Rizos, Helen

doi:10.1016/j.cell.2010.04.021

Cited by 59 publications

(67 citation statements)

References 47 publications

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“…IGFBP7 is a secreted protein recently proposed as a mediator of BRAF V600E -induced senescence in melanocytes (Wajapeyee et al 2008); this role, however, has been questioned by other authors (Scurr et al 2010). Interestingly, our recent results implicate IGFBP7 as a tumour suppressor protein in thyroid tumours: its expression is frequently lost in FTC and PTC, and its restoration modulates the transformed features of PTC-derived tumour cells (Vizioli et al 2010).…”

Section: G12vmentioning

confidence: 87%

“…INK4a and p21 CIP1 , two universally recognised OIS markers, and IGFBP7, a protein with an oncosuppressor role in thyroid tumours (Vizioli et al 2010), and often found involved in melanocyte OIS (Kortlever et al 2006, Acosta et al 2008, Kuilman et al 2008, Wajapeyee et al 2008, although its role in this process is controversial (Scurr et al 2010). Collectively, the three proteins were upregulated in PTMCs; the PTCs showed a variable pattern, including loss of expression; finally, the ATC sample was scored negative for the all proteins.…”

Section: Ink4amentioning

confidence: 93%

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Evidence of oncogene-induced senescence in thyroid carcinogenesis

Vizioli

Possik

Tarantino

et al. 2011

Endocrine-Related Cancer

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Oncogene-induced senescence (OIS) is a growth arrest triggered by the enforced expression of cancer-promoting genes and acts as a barrier against malignant transformation in vivo. In this study, by a combination of in vitro and in vivo approaches, we investigate the role of OIS in tumours originating from the thyroid epithelium. We found that expression of different thyroid tumour-associated oncogenes in primary human thyrocytes triggers senescence, as demonstrated by the presence of OIS hallmarks: changes in cell morphology, accumulation of SA-b-Gal and senescence-associated heterochromatic foci, and upregulation of transcription of the cyclindependent kinase inhibitors p16INK4a and p21 CIP1 . Furthermore, immunohistochemical analysis of a panel of thyroid tumours characterised by different aggressiveness showed that the expression of OIS markers such as p16 INK4a, p21 CIP1 and IGFBP7 is upregulated at early stages, and lost during thyroid tumour progression. Taken together, our results suggest a role of OIS in thyroid carcinogenesis.

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Section: G12vmentioning

confidence: 87%

Section: Ink4amentioning

confidence: 93%

Evidence of oncogene-induced senescence in thyroid carcinogenesis

Vizioli

Possik

Tarantino

et al. 2011

Endocrine-Related Cancer

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“…These findings have been confirmed by Bennett and coworkers (Gray-Schopfer et al 2006). Secreted IGFBP7 has been reported to play a central role in the initiation and maintenance of the senescent state of nevus cells (Wajapeyee et al 2008), but these findings were challenged recently Scurr et al 2010;Wajapeyee et al 2010).…”

Section: Ois In Models Of Nevus and Melanoma Formationmentioning

confidence: 99%

The essence of senescence: Figure 1.

Kuilman¹,

Michaloglou²,

Mooi³

et al. 2010

Genes Dev.

1,841

1,771

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Almost half a century after the first reports describing the limited replicative potential of primary cells in culture, there is now overwhelming evidence for the existence of “cellular senescence” in vivo. It is being recognized as a critical feature of mammalian cells to suppress tumorigenesis, acting alongside cell death programs. Here, we review the various features of cellular senescence and discuss their contribution to tumor suppression. Additionally, we highlight the power and limitations of the biomarkers currently used to identify senescent cells in vitro and in vivo.

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“…Nevertheless, a growing body of evidence supports the involvement of other pathways in the regulation of senescence, and in particular, in that of oncogene‐induced senescence (OIS) (Bianchi‐Smiraglia & Nikiforov, 2012; Christoffersen et al., 2010; Cipriano et al., 2011; Humbert et al., 2010; Lin et al., 2010; Scurr et al., 2010). …”

Section: Introductionmentioning

confidence: 99%

The SCN9A channel and plasma membrane depolarization promote cellular senescence through Rb pathway

et al. 2018

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SummaryOncogenic signals lead to premature senescence in normal human cells causing a proliferation arrest and the elimination of these defective cells by immune cells. Oncogene‐induced senescence (OIS) prevents aberrant cell division and tumor initiation. In order to identify new regulators of OIS, we performed a loss‐of‐function genetic screen and identified that the loss of SCN9A allowed cells to escape from OIS. The expression of this sodium channel increased in senescent cells during OIS. This upregulation was mediated by NF‐κB transcription factors, which are well‐known regulators of senescence. Importantly, the induction of SCN9A by an oncogenic signal or by p53 activation led to plasma membrane depolarization, which in turn, was able to induce premature senescence. Computational and experimental analyses revealed that SCN9A and plasma membrane depolarization mediated the repression of mitotic genes through a calcium/Rb/E2F pathway to promote senescence. Taken together, our work delineates a new pathway, which involves the NF‐κB transcription factor, SCN9A expression, plasma membrane depolarization, increased calcium, the Rb/E2F pathway and mitotic gene repression in the regulation of senescence. This work thus provides new insight into the involvement of ion channels and plasma membrane potential in the control of senescence.

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IGFBP7 Is Not Required for B-RAF-Induced Melanocyte Senescence

Cited by 59 publications

References 47 publications

Evidence of oncogene-induced senescence in thyroid carcinogenesis

Evidence of oncogene-induced senescence in thyroid carcinogenesis

The essence of senescence: Figure 1.

The SCN9A channel and plasma membrane depolarization promote cellular senescence through Rb pathway

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