Pathways of oncogene-induced senescence in human melanocytic cells

Bansal, Rajat; Nikiforov, Mikhail A.

doi:10.4161/cc.9.14.12251

Cited by 37 publications

(39 citation statements)

References 67 publications

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“…65 In contrast, depletion of p16 INK4A had no effect on senescence induced by oncogenic HRAS or NRAS in normal human melanocytes. 54,55,66 Based on all these data, it appears that the role of p53 and p16…”

Section: G12vmentioning

confidence: 95%

“…53 Three groups determined that p53 is dispensable for the senescence induced by activated HRAS or NRAS in normal human melanocytes. [54][55][56][57] Moreover, one of the groups demonstrated that a direct p53 target, p21 WAF/CIP , is also dispensable for the senescence induced by NRAS Q61K . 57 Additionally, normal human mammary epithelial cells were shown to undergo HRAS G12V -induced senescence via p53-independent mechanism.…”

Section: Are Tumor Suppressors Required For Ois?mentioning

confidence: 99%

“…Approximately 60% and 20% of human melanomas contain mutations in BRAF and NRAS, respectively, while mutations in HRAS are very rare. 55 The reasons for such heterogeneity are not completely understood.…”

Section: Different Types Of Oismentioning

confidence: 99%

“…[54][55][56][57] Instead, it has been demonstrated that OIS caused by the above oncogenes in human melanocytes could be at least partially abrogated by ectopic expression of the oncogenic transcription factor C-MYC 54 or by knockdown of its negative regulator PP2A-B56α, one of the subunits of PP2A tumor suppressor complex. 106 Intriguingly, despite similar degree of upregulation of C-MYC in all studied melanocytic populations, senescence phenotypes were effectively suppressed only in cells expressing BRAF V600E ; NRAS Q61R -induced senescence was affected only partially, and HRAS G12V -dependent senescence phenotypes remained unchanged.…”

Section: Different Types Of Oismentioning

confidence: 99%

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Controversial aspects of oncogene-induced senescence

Bianchi‐Smiraglia

Nikiforov

2012

Cell Cycle

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Section: G12vmentioning

confidence: 95%

Section: Are Tumor Suppressors Required For Ois?mentioning

confidence: 99%

Section: Different Types Of Oismentioning

confidence: 99%

Section: Different Types Of Oismentioning

confidence: 99%

See 2 more Smart Citations

Controversial aspects of oncogene-induced senescence

Bianchi‐Smiraglia

Nikiforov

2012

Cell Cycle

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“…Oncogene activation and the resulting aberrant proliferation induce another form of senescence called oncogene-induced senescence (OIS), which is considered one of the first barriers against tumor development (1, 3, 25–28). In many cases, OIS arises once cellular damage is ineffectively dealt with and unrepaired.…”

Section: Introductionmentioning

confidence: 99%

The Immortal Senescence

Bianchi‐Smiraglia

Lipchick

Nikiforov

2016

Methods in Molecular Biology

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Activation of oncogenic signaling paradoxically results in the permanent withdrawal from cell cycle and induction of senescence (oncogene-induced senescence (OIS)). OIS is a fail-safe mechanism used by the cells to prevent uncontrolled tumor-growth and, as such, it is considered as the first barrier against cancer. In order to progress, tumor cells thus need to first overcome the senescent phenotype. Despite the increasing attention gained by OIS in the past 20 years, this field is still rather young due to continuous emergence of novel pathways and processes involved in OIS. Among the many factors contributing to incomplete understanding of OIS are the lack of unequivocal markers for senescence and the complexity of the phenotypes revealed by senescent cells in in vivo and in vitro. OIS has been shown to play major roles at both the cellular and organismal levels in biological processes ranging from embryonic development to barrier to cancer progression. Here we will briefly outline major advances in methodologies that are being utilized for induction, identification and characterization of molecular processes in cells undergoing oncogene-induced senescence. The full description of such methodologies is provided in the corresponding chapters of the Book.

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Regulation of cellular senescence via the FOXO4‐p53 axis

Bourgeois

Madl

2018

FEBS Letters

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Forkhead box O (FOXO) and p53 proteins are transcription factors that regulate diverse signalling pathways to control cell cycle, apoptosis and metabolism. In the last decade both FOXO and p53 have been identified as key players in aging, and their misregulation is linked to numerous diseases including cancers. However, many of the underlying molecular mechanisms remain mysterious, including regulation of ageing by FOXOs and p53. Several activities appear to be shared between FOXOs and p53, including their central role in the regulation of cellular senescence. In this review, we will focus on the recent advances on the link between FOXOs and p53, with a particular focus on the FOXO4‐p53 axis and the role of FOXO4/p53 in cellular senescence. Moreover, we discuss potential strategies for targeting the FOXO4‐p53 interaction to modulate cellular senescence as a drug target in treatment of aging‐related diseases and morbidity.

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Pathways of oncogene-induced senescence in human melanocytic cells

Cited by 37 publications

References 67 publications

Controversial aspects of oncogene-induced senescence

Controversial aspects of oncogene-induced senescence

The Immortal Senescence

Regulation of cellular senescence via the FOXO4‐p53 axis

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