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BTG1 modulates ATF4 function in response to cellular stress: implications for tumor cell survival

ABSTRACT: Analysis of the effect of glutamine starvation in mouse embryonic fibroblasts (MEFs) with and without Btg1 at gene expression level. The hypothesis tested in the present study was that loss of Btg1 affect the expression of stress-response genes. Results provide important information of the differentially expressed genes regulated by Btg1 upon glutamine deprivation, explaining the survival advantage of tumor cells harboring Btg1 loss under cellular stress condition.

ORGANISM(S): Mus musculus

PROVIDER: GSE63642 | GEO | 2014/11/26

SECONDARY ACCESSION(S): PRJNA268518

REPOSITORIES: GEO

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BTG1 modulates ATF4 function in response to cellular stress: implications for tumor cell survival

Project description:Analysis of the effect of glutamine starvation in mouse embryonic fibroblasts (MEFs) with and without Btg1 at gene expression level. The hypothesis tested in the present study was that loss of Btg1 affect the expression of stress-response genes. Results provide important information of the differentially expressed genes regulated by Btg1 upon glutamine deprivation, explaining the survival advantage of tumor cells harboring Btg1 loss under cellular stress condition. Total RNA was obtained from WT and Btg1-/- MEFs subjected to 16 hours glutamine starvation compared to untreated cells.

2014-11-26 | E-GEOD-63642 | biostudies-arrayexpress

Oncogenic KRAS mediates amino acid metabolism during nutrient stress via regulation of NRF2 and ATF4 in NSCLC [shKRAS low Q]

Project description:Glutamine is a key nutrient for tumor cells that supports nucleotide and amino acid biosynthesis, replenishes the TCA cycle intermediates and contributes to redox metabolism. We identified oncogenic KRAS as a critical regulator of the response to glutamine deprivation in NSCLC. Full activation of the ATF4 stress response pathway is dependent on expression of NRF2 downstream of oncogenic KRAS in NSCLC. Through this mechanism, KRAS alters amino acid uptake and metabolism and sustains mTORC1 signaling during nutrient stress. Furthermore, we identified regulation of asparagine synthetase (ASNS) as a key effect of oncogenic KRAS signaling via ATF4 during glutamine deprivation, and a potential therapeutic target in KRAS mutant NSCLC.

2017-12-30 | GSE81643 | GEO

Oncogenic KRAS mediates amino acid metabolism during nutrient stress via regulation of NRF2 and ATF4 in NSCLC [shKRAS high Q]

2017-12-30 | GSE81642 | GEO

Oncogenic KRAS mediates amino acid metabolism during nutrient stress via regulation of NRF2 and ATF4 in NSCLC [low versus high Q]

2017-12-30 | GSE81641 | GEO

mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence [RNA-seq]

Project description:Quiescence is a cellular state in which cells undergo reversible cell cycle arrest in response to environmental challenges or lack of stimuli. When favorable conditions are engaged, the cells exit quiescence and start to proliferate. For example, quiescent stem cells and oocytes are activated by differentiation signals and fertilization, respectively. The regulation of quiescent state is also crucial for lymphocytes, such as T cells. Inappropriate activation of T cells often leads to autoimmune diseases and thus, the balance between quiescent and activated T cells must be preserved. Despite its importance, however, how T cells maintain the ‘quiescent state’ and exit from it remain largely unknown. Here, we identify BTG1 and BTG2 (BTG1/2) as factors responsible for T cell quiescence. Knockout of Btg1/2 in T cells resulted in a reduced threshold to T cell activation, increased proliferation and a concomitant reduction of the frequency of naive T cells. Loss of BTG1/2 rendered naive T cells to become spontaneously activated even without TCR stimuli. Interestingly, we found a global increase in mRNA abundance in naive T cells that lack BTG1/2. In addition, depletion of BTG1/2 led to an increase in mRNA half-life and poly(A) tail length. Thus, BTG1/2 promotes deadenylation and degradation of mRNA in naive T cells. Our study demonstrates a key mechanism underlying T cell quiescence, and suggests low mRNA abundance as a key feature for maintaining quiescent T cells.

2020-01-31 | GSE125865 | GEO

mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence [mTAIL-seq]

Project description:Quiescence is a cellular state in which cells undergo reversible cell cycle arrest in response to environmental challenges or lack of stimuli. When favourable conditions are engaged, the cells exit quiescence and start to proliferate. For example, quiescent stem cells and oocytes are activated by differentiation signals and fertilization, respectively. The regulation of quiescent state is also crucial for lymphocytes, such as T cells. Inappropriate activation of T cells often leads to autoimmune diseases and thus, the balance between quiescent and activated T cells must be preserved. Despite its importance, however, how T cells maintain the ‘quiescent state’ and exit from it remain largely unknown. Here, we identify BTG1 and BTG2 (BTG1/2) as factors responsible for T cell quiescence. Knockout of Btg1/2 in T cells resulted in a reduced threshold to T cell activation, increased proliferation and a concomitant reduction of the frequency of naive T cells. Loss of BTG1/2 rendered naive T cells to become spontaneously activated even without TCR stimuli. Interestingly, we found a global increase in mRNA abundance in naive T cells that lack BTG1/2. In addition, depletion of BTG1/2 led to an increase in mRNA half-life and poly(A) tail length. Thus, BTG1/2 promotes deadenylation and degradation of mRNA in naive T cells. Our study demonstrates a key mechanism underlying T cell quiescence, and suggests low mRNA abundance as a key feature for maintaining quiescent T cells.

2020-01-31 | GSE125889 | GEO

BTG1 mutation yields super-competitive B cells primed for malignant transformation

Project description:Mutations in the BTG1 tumor suppressor gene are exclusive to germinal center (GC)-derived B cell lymphomas and associate with low clinical outcome. To elucidate the effect of BTG1 mutations in mature B cells, we generated a mouse model for the conditional expression of mutant Btg1 Unlike conventional lymphoma oncogenes, mutated Btg1 expression in B cells did not induce GC hyperplasia. However, placing mutant and wild-type GC B cells in direct competition revealed that mutant Btg1 provides a massive advantage during the GC reaction. Furthermore, mutant Btg1 accelerates and dramatically increases the aggressiveness of BCL2-driven lymphomas in vivo. NGS, cellular and molecular profiling showed activation of Myc and mTORC1 anabolic programs in Btg1 mutant GC B cells, murine lymphomas and patient DLBCLs. These programs characterize T cell-selected GC B cells that enter a growth phase prior to clonal burst. We find that mutant Btg1 sensitizes GC B cells to T cell signals, resulting in a lower threshold to Myc activation, through mRNA translational biochemical mechanisms. Together, we link recurrent mutations of BTG1 to a massive fitness gain of GC B cells that confers an agressive and invasive phenotype to B cell lymphomas in vivo and associate with low clinical outcome in patients with agressive DLBCL. This work reveals a fine-tuned metabolic regulatory network that controls normal GC development and can be hijacked by lymphoma cells during disease progression. These findings have implications for fitness processes and natural selection at a broad level by providing fundamental insight into the power of subtle biochemical shifts to enhance biological fitness of cells.

2023-01-24 | GSE167786 | GEO

BTG1 regulates glucocorticoid receptor autoinduction in acute lymphoblastic leukemia

Project description:RNAi mediated knockdown of BTG1 in the acute lymphoblastic cell line RS4;11 causes this cell line to become resistant to prednisolone treatment when compared to control cells. In this experiment we treated BTG1 knockdown RS4;11 cells and control RS4;11 cells either with prednisolone or a vehicle control and compared the gene expression patterns of these cell lines. 8 samples were analyzed: we treated RS4;11 control or RS4;11 shRNA BTG1 cells with either prednisolone or vehicle control, the experiment was performed in duplicate. Genes with a > 2-fold change in expression after prednisolone treatment when compared to vehicle treatment were selected. Expression changes in BTG1 knockdown cells were compared to those in control vector transduced cells.

2010-06-23 | E-GEOD-18027 | biostudies-arrayexpress

BTG1 and BTG2 Regulate B Linege Commitment by Modulation of EBF1 Activity

Project description:The human BTG1 and BTG2 genes are targeted by genetic alterations in hematological malignancies. In this study we examined the unique and overlapping functions of Btg1 and Btg2 in mouse B cell development. Mice deficient for Btg1 and Btg2 displayed the strongest phenotype with a decrease in B cell numbers in bone marrow due to impaired B cell commitment and immature B cell differentiation. To determine the underlying mechanism, microarray expression analyis was performed on early (B220+ CD43+) and late (B220+ CD43-) B cells of WT and Btg1;Btg2 dKO mice.

2014-03-19 | GSE55997 | GEO

Loss of BTG1 function promotes ETV6-RUNX1-mediated leukemic transformation by upregulation of BCL6

Project description:Analysis of gene signatures in WT+Ctrl vs WT+ETV6-RUNX1, Btg1-/- and Btg1-/-+ETV6-RUNX1 in cKit+Ter119- fetal liver-derived hematopoietic progenitor cells (FL-HPCs). The Btg1-/-+ETV6-RUNX1 FL-HPCs display a strong increase in proliferation compared to WT+ETV6-RUNX1.

2014-08-22 | GSE60589 | GEO

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