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APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE245173 | GEO | 2024/12/06

REPOSITORIES: GEO

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APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma [SMART-Seq2]

Project description:Lung adenocarcinoma (LUAD) remains the leading cause of cancer deaths worldwide. Apurinic/apyrimidinic endonuclease 1 (APE1), an enzyme integral to DNA repair and redox signaling, is notably upregulated in various cancers, including LUAD. Here we reveal that APE1 amplification, primarily via allele duplication, correlates with poor prognosis in LUAD patients strongly. Using human LUAD cell models and a KRAS-driven genetically engineered mouse model (GEMM), we show that APE1 deletion hampers cell proliferation and tumor growth, highlighting its role in tumorigenesis. Mechanistically, APE1 promoted the transcription of urea cycle genes CPS1 and ARG2 by modulating the presence of G-quadruplex (G4) structures in their promoter regions. Loss of APE1 disrupts the urea cycle and pyrimidine metabolism, inducing metabolic reprogramming and growth arrest, which can be rescued by CPS1 or pyrimidine restoration. These findings uncover APE1’s role in metabolic regulation via G4-mediated transcription, providing a potential therapeutic target LUAD patients with elevated APE1 expression.

2024-12-06 | GSE245172 | GEO

APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma [RNA-seq]

2024-12-06 | GSE245168 | GEO

APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma [CUT&Tag]

2024-12-06 | GSE245167 | GEO

APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma [ATAC-seq]

2024-12-06 | GSE271726 | GEO

APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma

Project description:APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma

| PRJNA1027291 | ENA

APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma [CUT&Tag]

Project description:APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma [CUT&Tag]

| PRJNA1027294 | ENA

APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma [RNA-seq]

Project description:APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma [RNA-seq]

| PRJNA1027295 | ENA

APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma [SMART-Seq2]

Project description:APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma [SMART-Seq2]

| PRJNA1027298 | ENA

APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma [ATAC-seq]

Project description:APE1 regulates the transcription of urea cycle genes through stabilizing DNA G-quadruplexes in lung adenocarcinoma [ATAC-seq]

| PRJNA1132999 | ENA

FAIM regulates autophagy through glutaminolysis in lung adenocarcinoma.

Project description:Altered glutamine metabolism is an important aspect of cancer metabolic reprogramming. The GLS isoform GAC (glutaminase C), the rate-limiting enzyme in glutaminolysis, plays a vital role in cancer initiation and progression. Our previous studies demonstrated that phosphorylation of GAC was essential for its high enzymatic activity. However, the molecular mechanisms for GAC in maintaining its high enzymatic activity and protein stability still need to be further clarified. FAIM/FAIM1 (Fas apoptotic inhibitory molecule) is known as an important anti-apoptotic protein, but little is known about its function in tumorigenesis. Here, we found that knocking down FAIM induced macroautophagy/autophagy through suppressing the activation of the MTOR pathway in lung adenocarcinoma. Further studies demonstrated that FAIM could promote the tetramer formation of GAC through increasing PRKCE/PKCε-mediated phosphorylation. What's more, FAIM also stabilized GAC through sequestering GAC from degradation by protease ClpXP. These effects increased the production of α-ketoglutarate, leading to the activation of MTOR. Besides, FAIM also promoted the association of ULK1 and MTOR and this further suppressed autophagy induction. These findings discovered new functions of FAIM and elucidated an important molecular mechanism for GAC in maintaining its high enzymatic activity and protein stability.

| S-EPMC9225548 | biostudies-literature

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