Long noncoding RNA DLEU1 promotes proliferation and glycolysis of gastric cancer cells via APOC1 upregulation by recruiting SMYD2 to induce trimethylation of H3K4 modification

Xu, Haitao; Ba, Zhichang; Liu, Chunxun; Yu, Xuefeng

doi:10.1016/j.tranon.2023.101731

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2024

Publication Types

Select...

Article2

Preprint1

Relationship

Self Cite0

Independent3

Authors

Journals

Cited by 3 publications

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

Dexmedetomidine alleviates Hypoxia/reoxygenation-induced mitochondrial dysfunction in cardiomyocytes via activation of Sirt3/Prdx3 pathway

Tan,

Dong,

Wang

et al. 2024

DARU J Pharm Sci

View full text Add to dashboard Cite

Dexmedetomidine alleviates Hypoxia/reoxygenation-induced mitochondrial dysfunction in cardiomyocytes via activation of Sirt3/Prdx3 pathway

Tan,

Dong,

Wang

et al. 2024

DARU J Pharm Sci

View full text Add to dashboard Cite

Human disease-related long noncoding RNAs: Impact of ginsenosides

Jang,

Lee,

Kim

et al. 2024

Journal of Ginseng Research

View full text Add to dashboard Cite

EGF/APOC1/CPT1A Axis: A Novel Pathway in Gastric Cancer Metabolism and Therapeutic Targeting

Du,

Li,

Chen

et al. 2024

Preprint

View full text Add to dashboard Cite

Gastric cancer (GC) relies heavily on the reprogramming of lipid metabolism for energy, growth, and survival. Apolipoprotein C-I (APOC1) is implicated in the reprogramming of lipid metabolic processes in GC, yet the precise molecular mechanisms underlying this association remain incompletely understood. In this study, we identified APOC1 as a key player in GC metabolism and progression. Our findings show that APOC1 is upregulated in GC tissues and cells compared with controls and is correlated with poor prognosis. Furthermore, the overexpression of APOC1 promoted proliferation and migration, whereas the silencing of APOC1 led to decreased tumor growth and metastasis. Moreover, APOC1 was found to augment fatty acid oxidation (FAO) through its interaction with and regulation of carnitine palmitoyltransferase 1A (CPT1A). Disruption of APOC1 resulted in metabolic dysregulation, leading to mitochondrial oxidative stress. Conversely, the upregulation of APOC1 in GC cells promoted the catabolism of long-chain fatty acids, thereby facilitating tumor growth and migration. Mechanistically, APOC1 was shown to be regulated by epidermal growth factor (EGF), and its expression was directly targeted at the transcriptional level by AP-2α binding to its promoter region. Our research reveals a novel association between APOC1 and lipid metabolism, highlighting the EGF/APOC1/CPT1A axis as crucial factors in the progression of GC and potential targets for therapeutic interventions.

show abstract

Long noncoding RNA DLEU1 promotes proliferation and glycolysis of gastric cancer cells via APOC1 upregulation by recruiting SMYD2 to induce trimethylation of H3K4 modification

Cited by 3 publications

References 45 publications

Dexmedetomidine alleviates Hypoxia/reoxygenation-induced mitochondrial dysfunction in cardiomyocytes via activation of Sirt3/Prdx3 pathway

Dexmedetomidine alleviates Hypoxia/reoxygenation-induced mitochondrial dysfunction in cardiomyocytes via activation of Sirt3/Prdx3 pathway

Human disease-related long noncoding RNAs: Impact of ginsenosides

EGF/APOC1/CPT1A Axis: A Novel Pathway in Gastric Cancer Metabolism and Therapeutic Targeting

Contact Info

Product

Resources

About