Advancements in Activating Transcription Factor 5 Function in Regulating Cell Stress and Survival

Paerhati, Pameila; Liu, Jin; Jin, Zhedong; Jakoš, Tanja; Zhu, Shunyin; Lei, Qian; Jun, Zhu; Yuan, Yunsheng

doi:10.3390/ijms23137129

Cited by 10 publications

(6 citation statements)

References 95 publications

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“…The activating transcription factor 5 (ATF5) belongs to the family of cyclic adenosine monophosphate (cAMP) response element binding proteins. ATF5 has a crucial function in the control of cellular stress, as well as in cell differentiation, survival, and centrosome maintenance and development [ 53 ].…”

Section: Discussionmentioning

confidence: 99%

Enterotoxins A and B produced by Staphylococcus aureus increase cell proliferation, invasion and cytarabine resistance in acute myeloid leukemia cell lines

Turk,

Yanpar,

Baesmat

et al. 2023

Heliyon

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Section: Discussionmentioning

confidence: 99%

Enterotoxins A and B produced by Staphylococcus aureus increase cell proliferation, invasion and cytarabine resistance in acute myeloid leukemia cell lines

Turk,

Yanpar,

Baesmat

et al. 2023

Heliyon

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“…In addition to being a member of the basic leucine zipper transcription factor family, the JUN proto-oncogene belongs to the JUN family of immediate-early genes [ 27 ]. Regulatory proteins in the intracellular JUN family form homodimers or heterodimers with each other as well as with those in the FOS family, and they are closely related to the transcriptional regulation of many cytokines and growth factors in the cell [ 28 , 29 ]. Several malignant tumors express JUN, which is essential for regulating proliferation, apoptosis, and malignant transformation [ 30 , 31 ].…”

Section: Discussionmentioning

confidence: 99%

Terpinen-4-ol Induces Ferroptosis of Glioma Cells via Downregulating JUN Proto-Oncogene

Cao

Zeng

et al. 2023

Molecules

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According to previous research, turmeric seeds exhibit anti-inflammatory, anti-malignancy, and anti-aging properties due to an abundance of terpinen-4-ol (T4O). Although it is still unclear how T4O works on glioma cells, limited data exist regarding its specific effects. In order to determine whether or not glioma cell lines U251, U87, and LN229 are viable, CCK8 was used as an assay and a colony formation assay was performed using different concentrations of T4O (0, 1, 2, and 4 μM). The effect of T4O on the proliferation of glioma cell line U251 was detected through the subcutaneous implantation of the tumor model. Through high-throughput sequencing, a bioinformatic analysis, and real-time quantitative polymerase chain reactions, we identified the key signaling pathways and targets of T4O. Finally, for the measurement of the cellular ferroptosis levels, we examined the relationship between T4O, ferroptosis, and JUN and the malignant biological properties of glioma cells. T4O significantly inhibited glioma cell growth and colony formation and induced ferroptosis in the glioma cells. T4O inhibited the subcutaneous tumor proliferation of the glioma cells in vivo. T4O suppressed JUN transcription and significantly reduced its expression in the glioma cells. The T4O treatment inhibited GPX4 transcription through JUN. The overexpression of JUN suppressed ferroptosis in the cells rescued through T4O treatment. Taken together, our data suggest that the natural product T4O exerts its anti-cancer effects by inducing JUN/GPX4-dependent ferroptosis and inhibiting cell proliferation, and T4O will hope-fully serve as a prospective compound for glioma treatment.

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“…For instance, ATF5 can undergo ubiquitination, triggered by CDC34; and ATF5 degradation can be suppressed by cadmium and NLK phosphorylation, resulting in stabilization of ATF5 protein. ATF5 can also be degraded through proteasome pathways specifically in hepatocellular carcinoma cells; several miRNAs, such as miR-141-3p, miR-520b-3p, and miR-134-5p, have been identified to bind to the 3' UTR site of ATF5 mRNA and suppress ATF5 expression [38]. Future studies are needed to determine whether CRABP1 affects ATF5 protein stability.…”

Section: Discussionmentioning

confidence: 99%

Depleting Cellular Retinoic Acid Binding Protein 1 Impairs UPRmt

Wei,

Lerdall,

Najjar

et al. 2023

J Cell Signal

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Mitochondrial dysfunction underlines neurodegenerative diseases which are mostly characterized by progressive degeneration of neurons. We previously reported that Cellular retinoic acid Binding protein 1 (Crabp1) knockout (CKO) mice spontaneously developed age-dependent motor degeneration, with defects accumulated in spinal motor neurons (MNs), the only cell type in spinal cord that expresses CRABP1. Here we uncovered that mitochondrial DNA (mtDNA) content and the expression of genes involved in respiration were significantly reduced in CKO mouse spinal cord, accompanied by significantly elevated reactive oxygen species (ROS) and unfolded protein load, indicating that CRABP1 deficiency caused mitochondrial dysfunction. Further analyses of spinal cord tissues revealed significant reduction in the expression and activity of superoxide dismutase 2 (SOD2), as well as defected mitochondrial unfolded protein response (UPRmt) pathway, specifically an increase in ATF5 mRNA but not its protein level, which suggested failure in the translational response of ATF5 in CKO. Consistently, eukaryotic initiation factor-2α, (eIF2α) phosphorylation was reduced in CKO spinal cord. In a CRABP1 knockdown MN1 model, siCrabp1-MN1, we validated the cell-autonomous function of CRABP1 in modulating the execution of UPRmt. This study reveals a new functional role for CRABP1 in the execution of mitochondrial stress response, that CRABP1 modulates eIF2α phosphorylation thereby contributing to ATF5 translational response that is needed to mitigate mitochondria stress.

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Advancements in Activating Transcription Factor 5 Function in Regulating Cell Stress and Survival

Cited by 10 publications

References 95 publications

Enterotoxins A and B produced by Staphylococcus aureus increase cell proliferation, invasion and cytarabine resistance in acute myeloid leukemia cell lines

Enterotoxins A and B produced by Staphylococcus aureus increase cell proliferation, invasion and cytarabine resistance in acute myeloid leukemia cell lines

Terpinen-4-ol Induces Ferroptosis of Glioma Cells via Downregulating JUN Proto-Oncogene

Depleting Cellular Retinoic Acid Binding Protein 1 Impairs UPRmt

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