The p53 tumor suppressor: A master regulator of diverse cellular processes and therapeutic target in cancer

Farnebo, Marianne; Bykov, Vladimir J.N.; Wiman, Klas G.

doi:10.1016/j.bbrc.2010.02.152

Cited by 242 publications

(170 citation statements)

References 50 publications

Supporting

Mentioning

162

Contrasting

Unclassified

Order By: Relevance

“…Indeed, this transcription factor is well-known as a potent suppressor of tumor development by inhibiting cell-cycle progression and promoting senescence, apoptosis, or autophagy (32,33). More recently, accumulating evidence has pointed an alternative role of p53 by negatively regulating invasion and tumor cell metastasis (8,34,35).…”

Section: Discussionmentioning

confidence: 99%

Metformin Blocks Melanoma Invasion and Metastasis Development in AMPK/p53-Dependent Manner

Cerezo

Tichet

Abbe

et al. 2013

Molecular Cancer Therapeutics

184

139

View full text Add to dashboard Cite

Metformin was reported to inhibit the proliferation of many cancer cells, including melanoma cells. In this report, we investigated the effect of metformin on melanoma invasion and metastasis development. Using different in vitro approaches, we found that metformin inhibits cell invasion without affecting cell migration and independently of antiproliferation action. This inhibition is correlated with modulation of expression of proteins involved in epithelial-mesenchymal transition such as Slug, Snail, SPARC, fibronectin, and Ncadherin and with inhibition of MMP-2 and MMP-9 activation. Furthermore, our data indicate that this process is dependent on activation of AMPK and tumor suppressor protein p53. Finally, we showed that metformin inhibits melanoma metastasis development in mice using extravasation and metastasis models. The presented data reinforce the fact that metformin might be a good candidate for clinical trial in melanoma treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Metformin Blocks Melanoma Invasion and Metastasis Development in AMPK/p53-Dependent Manner

Cerezo

Tichet

Abbe

et al. 2013

Molecular Cancer Therapeutics

184

139

View full text Add to dashboard Cite

show abstract

“…p53 is inactivated in 10-12% of MM cases (Avet-Loiseau et al, 1999;Chng et al, 2007) resulting from either p53-DNA binding domain mutations or overexpression of murine double minute 2 gene (MDM2) (Farnebo et al, 2010). MDM2, an E3-ubiquitin ligase, binds p53 to ubiquitinate and targets it for degradation through ubiquitin/proteasome pathway (Piette et al, 1997).…”

Section: Deregulation Of Cell Cycle and Apoptosis Mechanismsmentioning

confidence: 99%

An update on molecular biology and drug resistance mechanisms of multiple myeloma

Mutlu

Kiraz

Gündüz

et al. 2015

Critical Reviews in Oncology/Hematology

View full text Add to dashboard Cite

Multiple myeloma (MM), a neoplasm of plasma cells, is the second most common hematological malignancy. Incidance rates increase after age 40. MM is most commonly seen in men and African-American population. There are several factors to this, such as obesity, environmental factors, family history, genetic factors and monoclonal gammopathies of undetermined significance (MGUS) that have been implicated as potentially etiologic. Development of MM involves a series of complex molecular events, including chromosomal abnormalities, oncogene activation and growth factor dysregulation. Chemotherapy is the most commonly used treatment strategy in MM. However, MM is a difficult disease to treat because of its marked resistance to chemotherapy. MM has been shown to be commonly multidrug resistance (MDR)-negative at diagnosis and associated with a high incidence of MDR expression at relapse. This review deals with the molecular aspects of MM, drug resistance mechanisms during treatment and also possible new applications for overcoming drug resistance. © 2015 Elsevier Ireland Ltd

show abstract

“…For example, the p53 pathway is activated by DNA damage and induces senescence and apoptosis through the Bax/Bc12 pathway [84].…”

Section: Molecular Mechanisms Underlying Induction Of Pluripotencymentioning

confidence: 99%

“…Knockdown of the p53 pathway or a main downstream target of the p53 pathway (i.e., p21) enhances the efficiency of iPSCs generation [78,80,[83][84][85][86]. The factor most likely responsible for success or failure to genetically reprogram somatic cells to an iPSC fate is likely c-Myc as it induces the production of oxidative stress radical oxygen species, which results in marked DNA damage.…”

Section: Molecular Mechanisms Underlying Induction Of Pluripotencymentioning

confidence: 99%

“…The factor most likely responsible for success or failure to genetically reprogram somatic cells to an iPSC fate is likely c-Myc as it induces the production of oxidative stress radical oxygen species, which results in marked DNA damage. Thus, culturing the cells in low oxygen culture condition [87] or in vitamin C supplement [88] improves iPSCs generating by inhibiting the up-regulation of p53 [84].…”

Section: Molecular Mechanisms Underlying Induction Of Pluripotencymentioning

confidence: 99%

See 1 more Smart Citation

Differentiation of Human Atrial Myocytes From Endothelial Progenitor Cell-Derived Induced Pluripotent Stem Cells

Jambi¹,

Ye²,

Gollob³

et al. 2013

Canadian Journal of Cardiology

View full text Add to dashboard Cite

The p53 tumor suppressor: A master regulator of diverse cellular processes and therapeutic target in cancer

Cited by 242 publications

References 50 publications

Metformin Blocks Melanoma Invasion and Metastasis Development in AMPK/p53-Dependent Manner

Metformin Blocks Melanoma Invasion and Metastasis Development in AMPK/p53-Dependent Manner

An update on molecular biology and drug resistance mechanisms of multiple myeloma

Differentiation of Human Atrial Myocytes From Endothelial Progenitor Cell-Derived Induced Pluripotent Stem Cells

Contact Info

Product

Resources

About