The Crosstalk and Clinical Implications of CircRNAs and Glucose Metabolism in Gastrointestinal Cancers

Cancers (Basel). 2023 Apr 10;15(8):2229. doi: 10.3390/cancers15082229.

Abstract

The majority of glucose in tumor cells is converted to lactate despite the presence of sufficient oxygen and functional mitochondria, a phenomenon known as the "Warburg effect" or "aerobic glycolysis". Aerobic glycolysis supplies large amounts of ATP, raw material for macromolecule synthesis, and also lactate, thereby contributing to cancer progression and immunosuppression. Increased aerobic glycolysis has been identified as a key hallmark of cancer. Circular RNAs (circRNAs) are a type of endogenous single-stranded RNAs characterized by covalently circular structures. Accumulating evidence suggests that circRNAs influence the glycolytic phenotype of various cancers. In gastrointestinal (GI) cancers, circRNAs are related to glucose metabolism by regulating specific glycolysis-associated enzymes and transporters as well as some pivotal signaling pathways. Here, we provide a comprehensive review of glucose-metabolism-associated circRNAs in GI cancers. Furthermore, we also discuss the potential clinical prospects of glycolysis-associated circRNAs as diagnostic and prognostic biomarkers and therapeutic targets in GI cancers.

Keywords: biomarkers; circular RNAs; gastrointestinal cancers; glucose metabolism; therapeutic targets.

Publication types

  • Review

Grants and funding

This work was supported in part by the National Natural Science Foundation of China (Grant Nos. 82173290 and 81871969), the Project of the Department of Education of Guangdong Province (Grant No. 2021KTSCX102) for Xiaojing Zhang; the National Natural Science Foundation of China (Grant Nos. 82172946 and 81772592) and a SZU Top Ranking Project (860-00000210) for Zhe Jin; the National Natural Science Foundation of China (Grant No. 82273029), Natural Science Foundation of Guangdong Province (2022A1515010706), and the Shenzhen Basic Research Fund (JCYJ20190808163801777) for Yin Peng.