Loss of Gadd45b accelerates BCR-ABL-driven CML

Sha, Xiaojin; Hoffman, Barbara; Liebermann, Dan A.

doi:10.18632/oncotarget.26076

Cited by 14 publications

(4 citation statements)

References 14 publications

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“…It is important to note that the human male germ cell line TCam-2 originates from seminoma, which is a type of TGCT [19]. In this context, it is worth noting that almost all NANOS1-repressed pro-apoptotic factors identified in this study (GADD45A, GADD45B, GADD45G, RHOB, and TP53BP2) are well-established tumor suppressors [27][28][29][30][31][32][33][34][35]. This is in line with NANOS1 itself being proposed to promote carcinogenesis [36].…”

Section: Discussionmentioning

confidence: 99%

Human NANOS1 Represses Apoptosis by Downregulating Pro-Apoptotic Genes in the Male Germ Cell Line

Janecki

Ilaslan

Smialek

et al. 2020

IJMS

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While two mouse NANOS paralogues, NANOS2 and NANOS3, are crucial for maintenance of germ cells by suppression of apoptosis, the mouse NANOS1 paralogue does not seem to regulate these processes. Previously, we described a human NANOS1 p.[(Pro34Thr);(Ser83del)] mutation associated with the absence of germ cells in seminiferous tubules of infertile patients, which might suggest an anti-apoptotic role of human NANOS1. In this study, we aimed to determine a potential influence of human NANOS1 on the maintenance of TCam-2 model germ cells by investigating proliferation, cell cycle, and apoptosis. Constructs encoding wild-type or mutated human NANOS1 were used for transfection of TCam-2 cells, in order to investigate the effect of NANOS1 on cell proliferation, which was studied using a colorimetric assay, as well as apoptosis and the cell cycle, which were measured by flow cytometry. RNA-Seq (RNA sequencing) analysis followed by RT-qPCR (reverse transcription and quantitative polymerase chain reaction) was conducted for identifying pro-apoptotic genes repressed by NANOS1. Here, we show that overexpression of NANOS1 downregulates apoptosis in TCam-2 cells. Moreover, we found that NANOS1 represses a set of pro-apoptotic genes at the mRNA level. We also found that the infertility-associated p.[(Pro34Thr);(Ser83del)] mutation causes NANOS1 to functionally switch from being anti-apoptotic to pro-apoptotic in the human male germ cell line. Thus, this report is the first to show an anti-apoptotic role of NANOS1 exerted by negative regulation of mRNAs of pro-apoptotic genes.

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Section: Discussionmentioning

confidence: 99%

Human NANOS1 Represses Apoptosis by Downregulating Pro-Apoptotic Genes in the Male Germ Cell Line

Janecki

Ilaslan

Smialek

et al. 2020

IJMS

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“…Several studies have examined the role of GADD45B in cancer, with some suggesting that it is up-regulated and involved in carcinogenesis through the DNA damage response [ 19 , 20 ]. However, other studies argue that GADD45B is down-regulated in human cancers that led to tumorigenesis and malignant progression [ 21 ]. Additionally, one study found that a high level of GADD45B significantly enhances chemosensitivity in prostate cancer and promotes cell apoptosis via the mitogen-activated protein kinase (MAPK) pathway [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

The down-regulation of GADD45B leads to a conversion of cellular oxidative phosphorylation to glycolysis and promotes the progression of bladder cancer

Wang,

Shen

et al. 2024

Heliyon

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“…GADD45B was abundant in the kidney, liver, and lung. GADD45B was controversial in cell stress response, and it may be protective or harmful [ 34 , 35 ]. FOSL2, FOS like 2, AP-1 transcription factor subunit, one of FOS proteins, was implicated as regulators of cell proliferation, differentiation, and transformation.…”

Section: Discussionmentioning

confidence: 99%

A nomogram for predicting metabolic steatohepatitis: The combination of NAMPT, RALGDS, GADD45B, FOSL2, RTP3, and RASD1

Liao

Zeng

et al. 2021

Open Medicine

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Objective To identify differentially expressed and clinically significant mRNAs and construct a potential prediction model for metabolic steatohepatitis (MASH). Method We downloaded four microarray datasets, GSE89632, GSE24807, GSE63067, and GSE48452, from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) analysis and weighted gene co-expression network analysis were performed to screen significant genes. Finally, we constructed a nomogram of six hub genes in predicting MASH and assessed it through receiver operating characteristic (ROC) curve, calibration plot, and decision curve analysis (DCA). In addition, qRT-PCR was used for relative quantitative detection of RNA in QSG-7011 cells to further verify the expression of the selected mRNA in fatty liver cells. Results Based on common DEGs and brown and yellow modules, seven hub genes were identified, which were NAMPT, PHLDA1, RALGDS, GADD45B, FOSL2, RTP3, and RASD1. After logistic regression analysis, six hub genes were used to establish the nomogram, which were NAMPT, RALGDS, GADD45B, FOSL2, RTP3, and RASD1. The area under the ROC of the nomogram was 0.897. The DCA showed that when the threshold probability of MASH was 0–0.8, the prediction model was valuable to GSE48452. In QSG-7011 fatty liver model cells, the relative expression levels of NAMPT, GADD45B, FOSL2, RTP3, RASD1 and RALGDS were lower than the control group. Conclusion We identified seven hub genes NAMPT, PHLDA1, RALGDS, GADD45B, FOSL2, RTP3, and RASD1. The nomogram showed good performance in the prediction of MASH and it had clinical utility in distinguishing MASH from simple steatosis.

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Loss of Gadd45b accelerates BCR-ABL-driven CML

Cited by 14 publications

References 14 publications

Human NANOS1 Represses Apoptosis by Downregulating Pro-Apoptotic Genes in the Male Germ Cell Line

Human NANOS1 Represses Apoptosis by Downregulating Pro-Apoptotic Genes in the Male Germ Cell Line

The down-regulation of GADD45B leads to a conversion of cellular oxidative phosphorylation to glycolysis and promotes the progression of bladder cancer

A nomogram for predicting metabolic steatohepatitis: The combination of NAMPT, RALGDS, GADD45B, FOSL2, RTP3, and RASD1

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