ASPP: a new family of oncogenes and tumour suppressor genes

Sullivan, Alice; Lü, Xin

doi:10.1038/sj.bjc.6603525

Cited by 175 publications

(160 citation statements)

References 38 publications

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“…It is unclear why p21 was upregulated whereas other p53 target genes such as PUMA and Noxa were not. Nevertheless, it is well known that there may be selective expression of p53 target genes due to cofactors such as the apoptosis stimulating proteins of p53 (Sullivan and Lu, 2007).…”

Section: Discussionmentioning

confidence: 99%

Temozolomide induces senescence but not apoptosis in human melanoma cells

et al. 2007

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Temozolomide (TMZ), a DNA alkylating agent used in the treatment of melanoma, is believed to mediate its effect by addition of a methyl group to the O 6 position of guanine in DNA. Resistance to the agent may be in part due to the activity of O 6 -methylguanine-DNA methyl transferase (MGMT). In the present study, we show that sensitivity of melanoma cells to TMZ was dependent on their p53 status and levels of MGMT. Analysis of the mechanisms underlying reduced viability showed no evidence for induction of apoptosis even though marked levels of apoptosis was seen in TK6 lymphoma cells. Sensitivity of melanoma cells was associated with p53-dependent G2/M cell cycle arrest and induction of senescence. To verify the role of p53, the assays were repeated in presence of pifithrin-a, an inhibitor of p53. This resulted in increased viability of melanoma cells with wild-type p53 and reversed G2/M cell cycle arrest. Paradoxically, apoptosis was increased in melanoma but decreased as expected in TK6 lymphoma cells. These results are consistent with the view that TMZ is relatively ineffective against melanoma due to defective apoptotic signalling resulting from activation of p53. The nature of the defects in apoptotic signalling remains to be explored.

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Section: Discussionmentioning

confidence: 99%

Temozolomide induces senescence but not apoptosis in human melanoma cells

et al. 2007

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“…For instance, ASPP1 and 2 (apoptosis stimulating proteins of p53) enhance the ability of p53 to stimulate specifically the expression of pro-apoptotic targets but not genes involved in cell cycle arrest. 44 Phosphorylation of p53 on serine 46 (Ser46) is another pertinent example. Until recently, this modification was correlated exclusively with induction of proapoptotic genes and triggering of cell death.…”

Section: Regulation Of Mirnas By P53mentioning

confidence: 99%

Tiny Actors, Great Roles: microRNAs in p53's Service

Raver-Shapira¹,

Oren²

2007

Cell Cycle

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“…Not surprisingly, altered expression of ASPP genes is a frequent event in tumors. 102 As ASPP proteins have different binding affinities for distinct p53 family members, 103 the development of competitor peptides potentially displacing iASPP from p53 and/or p73 may become a promising strategy to modulate ASPP functions in tumors.…”

Section: And References Therein)mentioning

confidence: 99%

p53-family proteins and their regulators: hubs and spokes in tumor suppression

2010

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The tumor suppressor p53 is a central hub in a molecular network controlling cell proliferation and death in response to potentially oncogenic conditions, and a wide array of covalent modifications and protein interactions modulate the nuclear and cytoplasmic activities of p53. The p53 relatives, p73 and p63, are entangled in the same regulatory network, being subject at least in part to the same modifications and interactions that convey signals on p53, and actively contributing to the resulting cellular output. The emerging picture is that of an interconnected pathway, in which all p53-family proteins are involved in the response to oncogenic stress and physiological inputs. Therefore, common and specific interactors of p53-family proteins can have a wide effect on function and dysfunction of this pathway. Many years of research have uncovered an impressive number of p53-interacting proteins, but much less is known about protein interactions of p63 and p73. Yet, many interactors may be shared by multiple p53-family proteins, with similar or different effects. In this study we review shared interactors of p53-family proteins with the aim to encourage research into this field; this knowledge promises to unveil regulatory elements that could be targeted by a new generation of molecules, and allow more efficient use of currently available drugs for cancer treatment.

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ASPP: a new family of oncogenes and tumour suppressor genes

Cited by 175 publications

References 38 publications

Temozolomide induces senescence but not apoptosis in human melanoma cells

Temozolomide induces senescence but not apoptosis in human melanoma cells

Tiny Actors, Great Roles: microRNAs in p53's Service

p53-family proteins and their regulators: hubs and spokes in tumor suppression

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