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Ezetimibe derivative L14-8 suppresses advanced prostate cancer by activating PLK1/TP53-SAT1-induced ferroptosis

ABSTRACT: Ezetimibe derivative L14-8 suppresses advanced prostate cancer by activating PLK1/TP53-SAT1-induced ferroptosis

PROVIDER: PRJNA1159398 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30628316_1.fastq.gz	Fastqsanger.gz
	SRR30628316_2.fastq.gz	Fastqsanger.gz
	SRR30628317_1.fastq.gz	Fastqsanger.gz
	SRR30628317_2.fastq.gz	Fastqsanger.gz
	SRR30628318_1.fastq.gz	Fastqsanger.gz

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Ezetimibe derivative L14-8 suppresses advanced prostate cancer by activating PLK1/TP53-SAT1-induced ferroptosis

Project description:Androgen receptor signaling inhibitors (ARSIs) have demonstrated a survival benefit in metastatic prostate cancer (PCa). However, patients taking these agents inevitably acquire resistance and even develop neuroendocrine prostate cancer (NEPC), in which stage, the AR signaling is inactive, and therapies are limited for these lethal cases. Therefore, there is an urgent need to develop novel treatments to improve patient outcomes. Here we report that L14-8, a small molecule derived and optimized from ezetimibe, significantly suppressed prostate cancer growth by inducing ferroptosis in vitro and in vivo without obvious toxicity. Further mechanism studies demonstrate that L14-8 bound to and enhanced the stability of PLK1 and promoted the phosphorylation and expression of TP53, which enhanced its enrichment at the promoter of SAT1, a ferroptosis inducer, and increased its transcriptional activity. Overall, our studies developed a novel anti-tumor agent for treating lethal prostate cancer in an AR-independent manner and provided mechanistic insights into its action by targeting the PLK1-mediated TP53-SAT1 axis-induced ferroptosis.

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Effects of deletion of SAT1, a polyamine-metabolic enzyme, on mouse HeLa xenograft tumor

Project description:An acidic tumor microenvironment plays a critical role in tumor progression. However, understanding of metabolic reprogramming of tumors in response to acidic extracellular pH has remained elusive. Using comprehensive metabolomic analyses, we demonstrated that acidic extracellular pH (pH 6.8) leads to the accumulation of N1-acetylspermidine, a pro-tumor metabolite, through upregulation of the expression of spermidine/spermine acetyl transferase 1 (SAT1). Inhibition of SAT1 expression suppressed the accumulation of intra- and extracellular N1-acetylspermidine at acidic pH. Conversely, overexpression 3 of SAT1 increased intra- and extracellular N1-acetylspermidine levels, supporting the proposal that SAT1 is responsible for accumulation of N1-acetylspermidine. While inhibition of SAT1 expression only had a minor effect on cancer cell growth in vitro, SAT1 knockdown significantly decreased tumor growth in vivo, supporting a contribution of the SAT1-N1-acetylspermidine axis to pro-tumor immunity. Immune cell profiling revealed that inhibition of SAT1 expression decreased neutrophil recruitment to the tumor, resulting in impaired angiogenesis and tumor growth. We showed that anti-neutrophil neutralizing antibodies suppressed growth in control tumors to a similar extent to that seen in SAT1 knockdown tumors in vivo. Further, a SAT1 signature was found to be correlated with poor patient prognosis. Our findings demonstrate that extracellular acidity stimulates recruitment of pro-tumor neutrophils via the SAT1-N1-acetylspermidine axis, which may represent a novel target for anti-tumor immune therapy.

2023-08-14 | GSE239784 | GEO

Genes regulated by SAT1 in brain tumors

Project description:Performed gene expression profiling of U87MG cells with two different shRNAs to SAT1 using Affymetrix microarrays covering 67,528 gene transcripts. Accordingly, we infected U87MG cells with lentiviruses expressing shRNAs to either the green fluorescent protein (GFP) or SAT1, performed a drug selection to ensure stable expression of the shRNAs, and expanded the cells for RNA harvest within 7 days of infection. RNA was reverse transcribed into cDNA, labelled with biotin and hybridized onto the arrays for analyses. Hierarchical clustering of duplicate experiments correctly segregated samples according to sample identity (i.e. shGFP clustered together, shSAT1-1 clustered together, and shSAT1-2 clustered together; with the latter two separately branching from shGFP)

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Streptomyces sp. SAT1

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Gene expression changes in testes from Abcg8 knockout mice compared to wild-type mice or to Abcg8 knockout mice where plant sterol entry was blocked by ezetimibe

Project description:Abcg8 knockout mice, fed chow, are infertile. These mice also are susceptible to absorption and retention of xenosterols contained in the diet. Ezetimibe, a blocker of dieary sterol entry, can reverse the fertility in Abcg8 knockout mice. In order to identify if the xenosterols resulted in disruption of a specific set of genes in the testes, we compared wild-type testes, Abcg8 knockout testes, or testes from Abcg8 knockout mice fed chow supplemented with 0.005% ezetimibe. To identify genes of interest, we reasoned that any causative gene expression changes seen in Abcg8 knockout mice fed chow, resulting in xenosterol exposure and accumulation, leading to infertilty, would be reveresed back to a pattern seen in the wild-type mice, when Abcg8 knockout mice are raised on chow containing ezetimibe (which prevents xenosterol absorption in the intestine). The target of this drug, Npc1l1, is not expressed in the testes. Testes from wild-type mice, Abcg8 knockout mice, and Abcg8 knockout mice fed chow supplemented with ezetimibe were analyzed.

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