TAp73 transcriptionally represses BNIP3 expression

Petrova, Varvara; Mancini, Mara; Agostini, Massimiliano; Knight, Richard; Annicchiarico-Petruzzelli, Margherita; Barlev, Nikolai A.; Melino, Gerry; Amelio, Ivano

doi:10.1080/15384101.2015.1044178

Cited by 17 publications

(13 citation statements)

References 117 publications

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“…A cooperation between p53 mutants and hypoxia-inducible factor-1 (HIF-1) determines the expression of fundamental components of the basal lamina, such as laminin-γ2 and collagen type VIIa1, in hypoxic tumours 41 . The result of the cooperation between the p53 mutant and HIF-1 is the generation of a protumorigenic microenvironment that facilitates the invasion of lung cancer cells and the growth of xenotransplanted tumours 41,54,55 . Remarkably, the trigger of this p53 mutant GOF requires hypoxia to initiate the HIF-1-mediated response; thus, again, a reciprocal interaction between extrinsic and intrinsic factors participates in the cascade of events (Fig.…”

Section: P53 Mutants Instruct the Microenvironmentmentioning

confidence: 99%

Context is everything: extrinsic signalling and gain-of-function p53 mutants

Amelio

Melino

2020

Cell Death Discov.

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The TP53 genomic locus is a target of mutational events in at least half of cancers. Despite several decades of study, a full consensus on the relevance of the acquisition of p53 gain-of-function missense mutants has not been reached. Depending on cancer type, type of mutations and other unidentified factors, the relevance for tumour development and progression of the oncogenic signalling directed by p53 mutants might significantly vary, leading to inconsistent observations that have fuelled a long and fierce debate in the field. Here, we discuss how interaction with the microenvironment and stressors might dictate the gain-of-function effects exerted by individual mutants. We report evidence from the most recent literature in support of the context dependency of p53 mutant biology. This perspective article aims to raise a discussion in the field on the relevance that context might have on p53 gain-offunction mutants, assessing whether this should generally be considered a cell non-autonomous process. Facts • Mutant p53 GOF effects have been shown to vary in different settings, potentially depending on cancer types, experimental models and conditions. • Reciprocal interaction between microenvironment and mutant p53 GOF effects exists.

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Section: P53 Mutants Instruct the Microenvironmentmentioning

confidence: 99%

Context is everything: extrinsic signalling and gain-of-function p53 mutants

Amelio

Melino

2020

Cell Death Discov.

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“…[40][41][42][43][44] The p73 locus encodes 2 types of transcription factors: full length pro-apoptotic isoforms (Tap73), and N-terminally truncated anti-apoptotic proteins (DNp73). DNp73 is frequently overexpressed in multiple primary tumor types and cancer cell lines, but is barely detected in normal human tissues.…”

Section: ¡418mentioning

confidence: 99%

Diallyl disulfide enhances carbon ion beams–induced apoptotic cell death in cervical cancer cells through regulating Tap73 /ΔNp73

Chen

Sun

et al. 2015

Cell Cycle

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Diallyl disulfide (DADS), extracted from crushed garlic by steam-distillation, has been reported to provide the anticancer activity in several cancer types. However, the effect of DADS on high-LET carbon beams -induced cell death remains unknown. Therefore, we used human cervical cancer cells to elucidate the molecular effects of this dallyl sulfide. Radiotherapy remains the mainstay of treatment, especially in advanced cervical cancer and there is still space to improve the radiosensitivity to reduce radiation dosage. In this study, we found that radiation effects evoked by high-LET carbon beam was marked by inhibition of cell viability, cell cycle arrest, significant rise of apoptotic cells, regulation of transcription factor, such as p73, as well as alterations of crucial mediator of the apoptosis pathway. We further demonstrated that pretreatment of 10 mM DADS in HeLa cells exposed to radiation resulted in decrease in cell viability and increased radiosensitivity. Additionally, cells pretreated with DADS obviously inhibited the radiationinduced G2/M phase arrest, but promoted radiation-induced apoptosis. Moreover, combination DADS and the radiation exacerbated the activation of apoptosis pathways through up-regulated ration of pro-apoptotic Tap73 to antiapoptotic DNp73, and its downstream proteins, such as FASLG, and APAF1. Taken together, these results suggest that DADS is a potential candidate as radio sensitive agent for cervical cancer.

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“…p53 family can be considered among the most powerful family of genes for the wide range of functions covering from tumour suppression, homeostasis and development [1][2][3][4][5][6][7][8][9][10][11]. In this context the p53 family member p73 plays critical roles such as tumour suppression [12][13][14][15][16][17], neuronal development and differentiation [18][19][20][21][22][23][24], metabolic control [25][26][27][28][29][30][31][32][33], and spermatogenesis and the maintenance of male and female fertility [34][35][36][37]. However, despite the important effort placed in investigating p73 functioning, a full dissections of its transcriptional programme and a clearly distinction of this from the transcriptome of its sibling p53 has not been completely elucidated.…”

Section: Introductionmentioning

confidence: 99%

Integrin-β4 is a novel transcriptional target of TAp73

Xie

Vikhreva

Annicchiarico-Petruzzelli

et al. 2018

Cell Cycle

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As a member of p53 family, p73 has attracted intense investigations due to its structural and functional similarities to p53. Among more than ten p73 variants, the transactivation (TA) domain-containing isoform TAp73 is the one that imitates the p53's behavior most. TAp73 induces apoptosis and cell cycle arrest, which endows it the capacity of tumour suppression. Also, it can exert diverse biological influences on cells through activating a complex and context dependent transcriptional programme. The transcriptional activities further broaden its roles in more intricate biological processes. In this article, we report that p73 is a positive regulator of a cell adhesion related gene named integrin β4 (ITGB4). This finding may have implications for the dissection of the biological mechanisms underlining p73 functions.

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TAp73 transcriptionally represses BNIP3 expression

Cited by 17 publications

References 117 publications

Context is everything: extrinsic signalling and gain-of-function p53 mutants

Context is everything: extrinsic signalling and gain-of-function p53 mutants

Diallyl disulfide enhances carbon ion beams–induced apoptotic cell death in cervical cancer cells through regulating Tap73 /ΔNp73

Integrin-β4 is a novel transcriptional target of TAp73

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