Crosstalk Between p53 and Mitochondrial Metabolism

Itahana, Koji; Pervaiz, Shazib

doi:10.1007/978-94-017-8984-4_12

Cited by 2 publications

(2 citation statements)

References 133 publications

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“…In our model, TGM2 contributes to a TP53-induced autophagy program and suppress transformation; however, TP53 has diverse roles in autophagy. Nuclear TP53 promotes autophagy through many of its target genes, such as DRAM1, C12orf5/TIGAR, DAPK1, SESN2/SESTRIN2, ULK1, ULK2, BBC3/PUMA, BAX, BAD , and BNIP3 ( Balaburski et al, 2010 ; Berkers et al, 2013 ; Itahana and Pervaiz, 2014 ; Levine and Abrams, 2008 ). On the other hand, cytoplasmic TP53 and mutant TP53 inhibit autophagy ( Berkers et al, 2013 ; Itahana and Pervaiz, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Transglutaminase 2 contributes to a TP53-induced autophagy program to prevent oncogenic transformation

Yeo

Itahana

Guo

et al. 2016

eLife

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Genetic alterations which impair the function of the TP53 signaling pathway in TP53 wild-type human tumors remain elusive. To identify new components of this pathway, we performed a screen for genes whose loss-of-function debilitated TP53 signaling and enabled oncogenic transformation of human mammary epithelial cells. We identified transglutaminase 2 (TGM2) as a putative tumor suppressor in the TP53 pathway. TGM2 suppressed colony formation in soft agar and tumor formation in a xenograft mouse model. The depletion of growth supplements induced both TGM2 expression and autophagy in a TP53-dependent manner, and TGM2 promoted autophagic flux by enhancing autophagic protein degradation and autolysosome clearance. Reduced expression of both CDKN1A, which regulates the cell cycle downstream of TP53, and TGM2 synergized to promote oncogenic transformation. Our findings suggest that TGM2-mediated autophagy and CDKN1A-mediated cell cycle arrest are two important barriers in the TP53 pathway that prevent oncogenic transformation.DOI: http://dx.doi.org/10.7554/eLife.07101.001

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Section: Discussionmentioning

confidence: 99%

Transglutaminase 2 contributes to a TP53-induced autophagy program to prevent oncogenic transformation

Yeo

Itahana

Guo

et al. 2016

eLife

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“…In the case of inefficient DNA repair, p53 triggers apoptosis via transcriptional induction of pro-apoptotic genes. In response to ROS, p53 additionally stimulates the expression of several genes coding for antioxidant enzymes such as SESN1/2, MnSOD, GPX, and others [141][142][143]. In line with this, the antioxidant, cytoprotective and pro-survival roles of p53 was demonstrated by Ding et al [144].…”

Section: Other Scenarios Of Set7/9-mediated Regulation Of Ros-induced...mentioning

confidence: 75%

Methyltransferase Set7/9 as a Multifaceted Regulator of ROS Response

Daks¹,

Shuvalov²,

Parfenyev³

et al. 2023

Int. J. Biol. Sci.

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Reactive oxygen species (ROS) induce multiple signaling cascades in the cell and hence play an important role in the regulation of the cell's fate. ROS can cause irreversible damage to DNA and proteins resulting in cell death. Therefore, finely tuned regulatory mechanisms exist in evolutionarily diverse organisms that are aimed at the neutralization of ROS and its consequences with respect to cellular damage. The SET domain-containing lysine methyltransferase Set7/9 (KMT7, SETD7, SET7, SET9) post-translationally modifies several histones and non-histone proteins via monomethylation of the target lysines in a sequence-specific manner. In cellulo, the Set7/9-directed covalent modification of its substrates affects gene expression, cell cycle, energy metabolism, apoptosis, ROS, and DNA damage response. However, the in vivo role of Set7/9 remains enigmatic. In this review, we summarize the currently available information regarding the role of methyltransferase Set7/9 in the regulation of ROS-inducible molecular cascades in response to oxidative stress. We also highlight the in vivo importance of Set7/9 in ROS-related diseases.

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Crosstalk Between p53 and Mitochondrial Metabolism

Cited by 2 publications

References 133 publications

Transglutaminase 2 contributes to a TP53-induced autophagy program to prevent oncogenic transformation

Transglutaminase 2 contributes to a TP53-induced autophagy program to prevent oncogenic transformation

Methyltransferase Set7/9 as a Multifaceted Regulator of ROS Response

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