Caspase recruitment domain family member 10 regulates carbamoyl phosphate synthase 1 and promotes cancer growth in bladder cancer cells

Liu, Xi; Zhang, Xiaolin; Bi, Jianbin; Li, Zhenhua; Zhang, Zhe; Kong, Chuize

doi:10.1111/jcmm.14683

Cited by 10 publications

(10 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CPS1 upregulation may be multi-faceted depending on the tissue of origin: in non-small-cell lung carcinomas, liver kinase B1/AMPK-mediated CPS1 transcriptional repression is lost, allowing the gene to be transcribed 48 . In bladder cancer, caspase recruitment domain family member 10 (CARD10), via nuclear factor kappa B (NF-κB), activates CPS1 expression 88 .…”

Section: Cps1 In Diseasementioning

confidence: 99%

CPS1: Looking at an ancient enzyme in a modern light

Nitzahn

Lipshutz

2020

Molecular Genetics and Metabolism

View full text Add to dashboard Cite

Section: Cps1 In Diseasementioning

confidence: 99%

CPS1: Looking at an ancient enzyme in a modern light

Nitzahn

Lipshutz

2020

Molecular Genetics and Metabolism

View full text Add to dashboard Cite

“…2 F) [ 28 ]. Besides, EMS altered the expression of apoptosis-related genes, such as the decrease expression of anti-apoptosis genes including TRAF2 [ 29 ], CARD10 [ 30 ], and the increase of pro-apoptosis gene expression including CASP3, RHOB [ 31 ], and FOXO3 [ 32 ] (Fig. 2 E).…”

Section: Resultsmentioning

confidence: 99%

Artificial exosomes mediated spatiotemporal-resolved and targeted delivery of epigenetic inhibitors

Lin

et al. 2021

J Nanobiotechnol

View full text Add to dashboard Cite

Background Malignant tumor is usually associated with epigenetic dysregulation, such as overexpression of histone deacetylase (HDAC), thus HDAC has emerged as a therapeutic target for cancer. Histone deacetylase inhibitor has been approved for clinical use to treat hematological cancers. However, the low solubility, short circulation lifetime, and high cytotoxicity partially limited their applications in solid tumor. Methods The upconversion nanoparticles (UC) modified with mesoporous silica (SUC) was used to load an HDACI, suberoylanilide hydroxamic acid (SAHA), and further camouflaged with M1 macrophage-derived exosome membranes (EMS). EMS was characterized in size and compositions. We also analyzed the epigenetic regulation induced by EMS. Furthermore, we evaluate the biodistribution and in vivo tumor inhibition after the systemic administration of EMS. Results This novel style spatiotemporal-resolved drug delivery system, EMS showed a high loading efficiency of SAHA. EMS could be taken up by lung cancer cells and lead to efficient epigenetic inhibition. We found that the integrin α4β1 on M1-EM, was crucial for the homing of EMS to tumor tissues for the first time. In tumor-bearing mice, EMS showed spatiotemporal-resolved properties and facilitated the drug accumulation in the tumors, which induced superior anti-tumor effects. Conclusion This novel style of spatiotemporal-resolved nanoparticles can be used as a theranostic platform for lung cancer therapy. Graphical Abstract

show abstract

“…Currently, we do not have data to show whether FMO3 regulates transcription of Cps1 or protein stability of it. Furthermore, it has been reported that NFKB, a transcription factor that can be activated by TMAO [15], induced expression of CPS1 in bladder tumor cell lines [88]. As the result, whether TMAO is involved in FMO3-regulated expression of Cps1 remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Proteomics-Based Identification of Interaction Partners of the Xenobiotic Detoxification Enzyme FMO3 Reveals Involvement in Urea Cycle

Zhao

Stemmer

Petriello

2022

Toxics

View full text Add to dashboard Cite

The hepatic xenobiotic metabolizing enzyme flavin-containing monooxygenase 3 (FMO3) has been implicated in the development of cardiometabolic disease primarily due to its enzymatic product trimethylamine-N oxide (TMAO), which has recently been shown to be associated with multiple chronic diseases, including kidney and coronary artery diseases. Although TMAO may have causative roles as a pro-inflammatory mediator, the possibility for roles in metabolic disease for FMO3, irrespective of TMAO formation, does exist. We hypothesized that FMO3 may interact with other proteins known to be involved in cardiometabolic diseases and that modulating the expression of FMO3 may impact on these interaction partners. Here, we combine a co-immunoprecipitation strategy coupled to unbiased proteomic workflow to report a novel protein:protein interaction network for FMO3. We identified 51 FMO3 protein interaction partners, and through gene ontology analysis, have identified urea cycle as an enriched pathway. Using mice deficient in FMO3 on two separate backgrounds, we validated and further investigated expressional and functional associations between FMO3 and the identified urea cycle genes. FMO3-deficient mice showed hepatic overexpression of carbamoylphosphate synthetase (CPS1), the rate-limiting gene of urea cycle, and increased hepatic urea levels, especially in mice of FVB (Friend leukemia virus B strain) background. Finally, overexpression of FMO3 in murine AML12 hepatocytes led to downregulation of CPS1. Although there is past literature linking TMAO to urea cycle, this is the first published work showing that FMO3 and CPS1 may directly interact, implicating a role for FMO3 in chronic kidney disease irrespective of TMAO formation.

show abstract

Caspase recruitment domain family member 10 regulates carbamoyl phosphate synthase 1 and promotes cancer growth in bladder cancer cells

Cited by 10 publications

References 36 publications

CPS1: Looking at an ancient enzyme in a modern light

CPS1: Looking at an ancient enzyme in a modern light

Artificial exosomes mediated spatiotemporal-resolved and targeted delivery of epigenetic inhibitors

Proteomics-Based Identification of Interaction Partners of the Xenobiotic Detoxification Enzyme FMO3 Reveals Involvement in Urea Cycle

Contact Info

Product

Resources

About