Olig2 SUMOylation protects against genotoxic damage response by antagonizing p53 gene targeting

Liu, Huiqing; Weng, Weiji; Guo, Rong–Jun; Zhou, Jie; Xue, Jun; Zhong, Shan; Cheng, Jinke; Zhu, Michael X.; Pan, Si Jian; Li, Yong

doi:10.1038/s41418-020-0569-1

Cited by 23 publications

(18 citation statements)

References 67 publications

(129 reference statements)

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“…An important pathway enriched with linseed supplementation is the P53 signaling pathway, which is involved in damage repair and cell proliferation [ 46 ]. Some of the up-regulated genes ( APAF3, CCNG1, CCNG2 and PPM1D ) are intermediates for P53 activity, which is involved in cellular growth arrest, apoptosis, angiogenesis and DNA repair [ 47 ]. Our data demonstrated that linseed supplementation promotes mammalian anti-cancer activity as reported in previous studies [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Transcriptome Adaptation of the Ovine Mammary Gland to Dietary Supplementation of Extruded Linseed

Conte

Giordani

Vangelisti

et al. 2021

Animals

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Several dietary strategies were adopted to reduce saturated fatty acids and increase beneficial fatty acids (FA) for human health. Few studies are available about the pathways/genes involved in these processes. Illumina RNA-sequencing was used to investigate changes in the ovine mammary gland transcriptome following supplemental feeding with 20% extruded linseed. Comisana ewes in mid-lactation were fed a control diet for 28 days (control period) followed by supplementation with 20% DM of linseed panel for 28 days (treatment period). Milk production was decreased by 30.46% with linseed supplementation. Moreover, a significant reduction in fat, protein and lactose secretion was also observed. Several unsaturated FAs were increased while short and medium chain saturated FAs were decreased by linseed treatment. Around four thousand (1795 up- and 2133 down-regulated) genes were significantly differentially regulated by linseed supplementation. The main pathways affected by linseed supplementation were those involved in the energy balance of the mammary gland. Principally, the mammary gland of fed linseed sheep showed a reduced abundance of transcripts related to the synthesis of lipids and carbohydrates and oxidative phosphorylation. Our study suggests that the observed decrease in milk saturated FA was correlated to down-regulation of genes in the lipid synthesis and lipid metabolism pathways.

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Section: Discussionmentioning

confidence: 99%

Transcriptome Adaptation of the Ovine Mammary Gland to Dietary Supplementation of Extruded Linseed

Conte

Giordani

Vangelisti

et al. 2021

Animals

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“…However, even in the absence of p53, cancer cells are still able to halt cell cycle in response to genotoxic stimuli [ 180 , 181 ]. It was shown that in response to chemotherapeutic agents, cell cycle arrest and apoptosis are p73 dependent [ 71 , 156 , 157 , 182 ].…”

Section: P73 and Hallmarks Of Cancermentioning

confidence: 99%

The p53 family member p73 in the regulation of cell stress response

et al. 2021

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During oncogenesis, cells become unrestrictedly proliferative thereby altering the tissue homeostasis and resulting in subsequent hyperplasia. This process is paralleled by resumption of cell cycle, aberrant DNA repair and blunting the apoptotic program in response to DNA damage. In most human cancers these processes are associated with malfunctioning of tumor suppressor p53. Intriguingly, in some cases two other members of the p53 family of proteins, transcription factors p63 and p73, can compensate for loss of p53. Although both p63 and p73 can bind the same DNA sequences as p53 and their transcriptionally active isoforms are able to regulate the expression of p53-dependent genes, the strongest overlap with p53 functions was detected for p73. Surprisingly, unlike p53, the p73 is rarely lost or mutated in cancers. On the contrary, its inactive isoforms are often overexpressed in cancer. In this review, we discuss several lines of evidence that cancer cells develop various mechanisms to repress p73-mediated cell death. Moreover, p73 isoforms may promote cancer growth by enhancing an anti-oxidative response, the Warburg effect and by repressing senescence. Thus, we speculate that the role of p73 in tumorigenesis can be ambivalent and hence, requires new therapeutic strategies that would specifically repress the oncogenic functions of p73, while keeping its tumor suppressive properties intact.

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“…In fact, p53 is an excellent target as public neoantigen, considering that it is by far the most frequently mutated gene [31][32][33][34] and it has roles in regulating crucial factors in cancer biology such as cell death [35][36][37][38][39], cell cycle [40], cell metabolism [41][42][43][44][45][46][47][48], as well as commensal microbes [20,[49][50][51]. This is in keeping the function of the other members of the same family, namely p63 and p73 [52][53][54][55][56][57][58][59]; and with the ability to predict overall cancer patient survival [60][61][62] as other prognostic factors in cancer progression [27,63,64].…”

Section: Bispecific Antibodies As An Innovative Cancer Immunotherapymentioning

confidence: 99%

Recent advances in cancer immunotherapy

et al. 2021

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Cancer immunotherapy represents a major advance in the cure of cancer following the dramatic advancements in the development and refinement of chemotherapies and radiotherapies. In the recent decades, together with the development of early diagnostic techniques, immunotherapy has significantly contributed to improving the survival of cancer patients. The immune-checkpoint blockade agents have been proven effective in a significant fraction of standard therapy refractory patients. Importantly, recent advances are providing alternative immunotherapeutic tools that could help overcome their limitations. In this mini review, we provide an overview on the main steps of the discovery of classic immune-checkpoint blockade agents and summarise the most recent development of novel immunotherapeutic strategies, such as tumour antigens, bispecific antibodies and TCR-engineered T cells.

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Olig2 SUMOylation protects against genotoxic damage response by antagonizing p53 gene targeting

Cited by 23 publications

References 67 publications

Transcriptome Adaptation of the Ovine Mammary Gland to Dietary Supplementation of Extruded Linseed

Transcriptome Adaptation of the Ovine Mammary Gland to Dietary Supplementation of Extruded Linseed

The p53 family member p73 in the regulation of cell stress response

Recent advances in cancer immunotherapy

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