ArticleCell death & disease2023
Fasting regulates mitochondrial function through lncRNA PRKCQ-AS1-mediated IGF2BPs in papillary thyroid carcinoma.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Glucose Metabolic Reprogramming in Thyroid Cancer: Underlying Molecular Mechanisms and Links to Progression and Treatment.Current medical science · 2026Review
- Analysis of the mechanism and prognostic value of PRKCQ-AS1 in inhibiting the progression of lung adenocarcinoma via regulating the PD-1/PD-L1 pathway.Scientific reports · 2026Article
- Role of HOXA transcript antisense RNA myeloid-specific 1 in cancer (Review).Oncology letters · 2026Review
- The Emerging Role of Mitochondrial Dysfunction in Thyroid Cancer: Mediating Tumor Progression, Drug Resistance, and Reshaping of the Immune Microenvironment.Biomolecules · 2025Review
- Clinical significance and biological function of PRKCQ-AS1/miR-582-3p expression in LUAD.Hereditas · 2025Article
- Intermittent Fasting and Fasting-mimicking Diet: Promising Strategies in Cancer Management.Current medicinal chemistry · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Recurring evidence suggests that fasting has extensive antitumor effects in various cancers, including papillary thyroid carcinoma (PTC). However, the underlying mechanism of this relationship with PTC is unknown. In this study, we study the effect of fasting on glycolysis and mitochondrial function in PTC. We find that fasting impairs glycolysis and reduces mitochondrial dysfunction in vitro and in vivo and also fasting in vitro and fasting mimicking diets (FMD) in vivo significantly increase the expression of lncRNA-protein kinase C theta antisense RNA 1 (PRKCQ-AS1), during the inhibition of TPC cell glycolysis and mitochondrial function. Moreover, lncRNA PRKCQ-AS1 was significantly lower in PTC tissues and cells. In addition, PRKCQ-AS1 overexpression increased PTC cell glycolysis and mitochondrial function; PRKCQ-AS1 knockdown has the opposite effect. On further mechanistic analysis, we identified that PRKCQ-AS1 physically interacts with IGF2BPs and enhances protein arginine methyltransferases 7 (PRMT7) mRNA, which is the key player in regulating glycolysis and mitochondrial function in PTC. Hence, PRKCQ-AS1 inhibits tumor growth while regulating glycolysis and mitochondrial functions via IGF2BPs/PRMT7 signaling. These results indicate that lncRNA PRKCQ-AS1 is a key downstream target of fasting and is involved in PTC metabolic reprogramming. Further, the PRKCQ-AS1/IGF2BPs/PRMT7 axis is an ideal therapeutic target for PTC diagnosis and treatment.
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