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Colorectal cancer (CRC), a common tumor, is characterized by a high mortality rate. Long non-coding RNA  maternally expressed gene 3 (MEG3)  serves a regulatory role in the carcinogenesis and progression of several types of cancer; however, its role in CRC remains largely unknown. The aim of this study was to explore the regulatory role and mechanism(s) of  MEG3  in CRC. The Warburg effect or aerobic glycolysis is characteristic of the metabolism of tumor cells. To determine the effect of  MEG3  on glycolysis of CRC cells, we used an XF analyzer to perform glycolysis stress test assays and found that overexpression of MEG3 significantly inhibited glycolysis, glycolytic capacity, as well as lactate production in CRC cells, whereas knockdown of MEG3 produced the opposite effect. Mechanistically, overexpression of MEG3 induced ubiquitin-dependent degradation of c-Myc and inhibited c-Myc target genes involved in the glycolysis pathway such as lactate dehydrogenase A, pyruvate kinase muscle 2, and hexokinase 2. Moreover, we found that  MEG3  can be activated by vitamin D and vitamin D receptor (VDR). Clinical data demonstrated that  MEG3  was positively associated with serum vitamin D concentrations in patients with CRC. We found that 1,25(OH) 2 D 3  treatment increased  MEG3  expression, and knockdown of VDR abolished the effect of MEG3 on glycolysis. These results indicate that vitamin D-activated  MEG3  suppresses aerobic glycolysis in CRC cells  via  degradation of c-Myc. Thus, vitamin D may have therapeutic value in the treatment of CRC.

Long Non-coding RNA MEG3 Activated by Vitamin D Suppresses Glycolysis in Colorectal Cancer via Promoting c-Myc Degradation