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Melatonin inhibited tumorigenesis of bladder cancer via suppressing PPARγ/ENO1 mediated glycolysis

ABSTRACT: Melatonin inhibited tumorigenesis of bladder cancer via suppressing PPARγ/ENO1 mediated glycolysis

PROVIDER: PRJNA876233 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21403389_1.fastq.gz	Fastqsanger.gz
	SRR21403389_2.fastq.gz	Fastqsanger.gz
	SRR21403390_1.fastq.gz	Fastqsanger.gz
	SRR21403390_2.fastq.gz	Fastqsanger.gz
	SRR21403391_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Melatonin inhibited tumorigenesis of bladder cancer via suppressing PPARγ/ENO1 mediated glycolysis

Project description:Bladder cancer (BLCA) is one of the most malignant human cancers in the world. The increasingly prominent phenomenon of chemoresistance has become an essential obstacle to clinical treatment for BLCA, and there is an urgent need to explore novel drugs to improve the current clinical status. Melatonin is a well-known natural hormone that showed a potential anti-cancer effect in multiple human cancers. In our study, we comprehensively explored the inhibitory effect of melatonin on BLCA and found that it could suppress the glycolysis process in BLCA cells. Moreover, we discovered that the ninth step enzyme ENO1 of glycolysis was the downstream effector of melatonin and could be a predictive biomarker of BLCA patients.

2022-09-06 | GSE212599 | GEO

Melatonin inhibits bladder tumorigenesis by suppressing PPARγ/ENO1-mediated glycolysis.

Project description:Melatonin is a well-known natural hormone, which shows a potential anticancer effect in many human cancers. Bladder cancer (BLCA) is one of the most malignant human cancers in the world. Chemoresistance is an increasingly prominent phenomenon that presents an obstacle to the clinical treatment of BLCA. There is an urgent need to investigate novel drugs to improve the current clinical status. In our study, we comprehensively explored the inhibitory effect of melatonin on BLCA and found that it could suppress glycolysis process. Moreover, we discovered that ENO1, a glycolytic enzyme involved in the ninth step of glycolysis, was the downstream effector of melatonin and could be a predictive biomarker of BLCA. We also proved that enhanced glycolysis simulated by adding exogenous pyruvate could induce gemcitabine resistance, and melatonin treatment or silencing of ENO1 could intensify the cytotoxic effect of gemcitabine on BLCA cells. Excessive accumulation of reactive oxygen species (ROS) mediated the inhibitory effect of melatonin on BLCA cells. Additionally, we uncovered that PPARγ was a novel upstream regulator of ENO1, which mediated the downregulation of ENO1 caused by melatonin. Our study offers a fresh perspective on the anticancer effect of melatonin and encourages further studies on clinical chemoresistance.

| S-EPMC10079981 | biostudies-literature

ENO1 influences ATP pool of cytoplasm and lactate homeostasis by regulating glycolysis to promote tumor stemness and metastasis

Project description:This study demonstrated the role of the glycolytic enzyme alpha-enolase (ENO1) on glycolysis and stemness in gastric cancer (GC). High ENO1 expression was associated with poor prognosis and promoted malignant phenotypes and stem-like characteristics in GC. Mechanistically, ENO1 directly stimulated lactate and ATP production by regulating glycolysis, affecting lactate homeostasis and intracellular ATP pools, and co-regulating the AMPK/mTOR and PI3K/AKT signaling pathways. This ultimately drove GC stemness, epithelial-mesenchymal transition (EMT)-related markers, self-renewal, migration, and invasion.

2025-09-27 | GSE307717 | GEO

Single-gastruloid trancriptomics: control vs glycolysis inhibited at 48h and 96h post-aggregation

Project description:Bulk RNA seq of single gastruloids at 48h post-aggregation and 96h post-aggregation. Two different conditions were compared: control vs glycolysis inhibited (6mM 2-deoxy-D-glucosebetween, 24h-48h post aggregation). Aim of the study was to determine short-term effects of glycolysis inhibition on transcription, especially components of signalling pathways, and long-term effects on cell type proportions.

2025-04-10 | E-MTAB-13543 | biostudies-arrayexpress

PCNA regulates metabolism by stabilizing ENO1 and 6PGD

Project description:The essential roles of PCNA as a scaffold protein in DNA replication and repair are well established, while its more recently discovered cytosolic roles are less explored. Alpha-enolase (ENO1) and 6-phosphogluconate dehydrogenase (6PGD), important proteins in glycolysis and the Pentose Phosphate Pathway (PPP), respectively, both contain PCNA interacting motifs. Here we show reduced binding to PCNA when the PCNA interacting motif APIM in ENO1 is mutated. Mutant cells have lower ENO1 protein levels, have reduced glucose consumption, altered glycolytic metabolite and nucleoside phosphate pools and increased activation of the citric acid cycle (TCA) compared to parental cells. Treatment of a panel of haematological cell lines with a cell penetrating peptide containing APIM (ATX-101), lead to a metabolic shift with reduction in glycolytic metabolite and nucleoside phosphate pools as well reduced levels of ENO1 and 6PGD proteins. These results suggests that PCNA stabilize ENO1 and 6PGD, and that targeting PCNA reduce the glycolysis, PPP and nucleoside phosphate pools via destabilization of these proteins.

2023-03-10 | PXD028314 | Pride

Melatonin inhibits fibroblast cell functions and hypertrophic scar formation by enhancing autophagy through the MT2 receptor-inhibited PI3K/Akt /mTOR signaling

Project description:Hypertrophic scar (HS) is a fibrotic skin condition and characterized by abnormal proliferation of myofibroblasts and accumulation of extracellular matrix. Melatonin, an endogenous hormone, can alleviate fibrosis in multiple models of diseases. This study examined the effect of melatonin on fibrosis in primary fibroblasts from human HS (HSFs) and a rabbit ear model and potential mechanisms. Melatonin treatment significantly decreased the migration and contraction capacity, collagen and α-smooth muscle actin (α-SMA) production in HSFs. RNA-sequencing and bioinformatic analyses indicated that melatonin modulated the expression of genes involved in autophagy and oxidative stress. Mechanistically, melatonin treatment attenuated the AKT/mTOR activation through affecting the binding of MT2 receptor with PI3K to enhance autophagy, decreasing fibrogenic factor production in HSFs. Moreover, melatonin treatment inhibited HS formation in rabbit ears by enhancing autophagy. The anti-fibrotic effects of melatonin were abrogated by treatment with an autophagy inhibitor (3-methyladenine, 3-MA), an Akt activator (SC79), or an MT2 selective antagonist (4-phenyl-2propionamidotetralin, 4-P-PDOT). Therefore, melatonin may be a potential drug for prevention and treatment of HS.

2022-06-03 | GSE190135 | GEO

ENO1 siRNA knockdown in Human HeLa cells

Project description:HeLa cells were either treated with ENO1 or control siRNAs using the protocol of the RNAiMax reagent (ENO1 pool: SMARTpool ON-TARGETplus L-004034-00-0005 and control pool: ON-TARGETplus non-targeting siRNAs 1-4). Three replicates per condition were produced.

2020-10-27 | E-MTAB-9032 | biostudies-arrayexpress

ENO1 promotes liver carcinogenesis through YAP1-dependent arachidonic acid metabolism

Project description:Enolase 1 (ENO1) is a glycolytic enzyme that plays essential roles in various pathological activities including cancer development. However, the mechanisms underlying ENO1-contributed tumorigenesis are not well explained. Here, we uncover that ENO1, as an RNA-binding protein, binds to the cytosine-uracil-guanine-rich elements of YAP1 messenger RNA to promote its translation. ENO1 and YAP1 positively regulate alternative arachidonic acid (AA) metabolism by inverse regulation of PLCB1 and HPGD (15-hydroxyprostaglandin dehydrogenase). The YAP1/PLCB1/HPGD axis-mediated activation of AA metabolism and subsequent accumulation of prostaglandin E2 (PGE2) are responsible for ENO1-mediated cancer progression, which can be retarded by aspirin. Finally, aberrant activation of ENO1/YAP1/PLCB1 and decreased HPGD expression in clinical hepatocellular carcinoma samples indicate a potential correlation between ENO1-regulated AA metabolism and cancer development. These findings underline a new function of ENO1 in regulating AA metabolism and tumorigenesis, suggesting a therapeutic potential for aspirin in patients with liver cancer with aberrant expression of ENO1 or YAP1.

2023-05-19 | GSE183703 | GEO

Exon Skipping of Ste20-Like Kinase Enhances Glycolysis and Tumor Progression by Activating Enolase 1 mediated Phosphoenolpyruvate Production

Project description:Dysregulated RNA splicing is activated in tumors; however, the metabolic landscape and consequent implications of this process remain largely unexplored. In this study, we identified exon skipping in Ste20-like kinase (SLK), resulting in a variant isoform of SLK (SLKv), which promotes glycolysis in tumor cells. Mechanistically, SLKv enhances the activity of enolase 1 (ENO1) by binding and phosphorylating the ENO1 serine 2 residue. This modification increases the efficiency of ENO1 in catalyzing the production of phosphoenolpyruvate (PEP). Notably, the accumulation of PEP further accelerates glycolysis by binding to and activating the glycolytic enzyme hexokinase 2 (HK2), phosphofructokinase muscle (PFKM), and phosphoglycerate mutase 1 (PGAM1). Meanwhile, transforming growth factor β (TGFβ) promotes exon skipping of SLK by upregulating the splicing factor KH RNA binding domain containing, signal transduction associated 1 (KHDRBS1). The application of antisense oligonucleotides (ASO) that target SLKv hinders glycolysis and tumorigenesis. These findings establish SLKv as a critical promoter of glycolysis and present a novel metabolic target for cancer therapy.

2025-06-17 | GSE299345 | GEO

Effect of PPARγ inhibition on pulmonary endothelial cell gene expression: Gene profiling in pulmonary hypertension

Project description:The loss of PPARγ is found to be associated with the development of pulmonary hypertension (PH). We hypothesize that PPARγ inhibition induced gene expression changes may underscore the endothelial dysfunction in the disease process. We utilized microarray analysis to determine gene expression changes in PPARγ inhibited ovine PAECs. Ovine PAECs were treated with vehicle (DMSO) or GW9662 (5μM) for 24hrs, and total RNA was extracted for microarray analysis.

2009-12-27 | E-GEOD-14546 | biostudies-arrayexpress

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