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Long noncoding RNA AGPG regulates PFKFB3-mediated tumor glycolytic reprogramming
Jia Liu1, Ze-Xian Liu1, Qi-Nian Wu1
1State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Nature Communications
|March 22, 2020
Summary
The long noncoding RNA Actin Gamma 1 Pseudogene (AGPG) promotes cancer cell growth by stabilizing the PFKFB3 protein, increasing glycolysis. Inhibiting AGPG shows promise for esophageal cancer therapy.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Tumor cells exhibit metabolic reprogramming to support rapid proliferation.
- The function of long noncoding RNAs (lncRNAs) in cancer metabolism is not fully understood.
Purpose of the Study:
- To investigate the role of lncRNAs in metabolic reprogramming in esophageal squamous cell carcinoma (ESCC).
- To elucidate the mechanism by which lncRNAs influence cancer metabolism and proliferation.
Main Methods:
- Screening of lncRNAs involved in glycolysis and cell proliferation in ESCC.
- Investigating the interaction between AGPG and PFKFB3 using biochemical assays.
- Assessing the effect of AGPG inhibition on tumor growth in patient-derived xenograft (PDX) models.
Main Results:
- The lncRNA Actin Gamma 1 Pseudogene (AGPG) was identified as crucial for enhanced glycolysis and proliferation in ESCC.
- AGPG binds to and stabilizes PFKFB3 by preventing its proteasomal degradation, leading to increased glycolytic flux.
- Loss or mutation of TP53 results in the upregulation of AGPG.
- Inhibition of AGPG significantly reduced tumor growth in PDX models.
Conclusions:
- AGPG promotes cancer cell proliferation by stabilizing PFKFB3 and enhancing glycolysis.
- AGPG is a transcriptional target of p53, and its expression is upregulated upon TP53 loss.
- AGPG is a potential therapeutic target and biomarker for esophageal squamous cell carcinoma and other cancers.
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