J Cancer 2018; 9(14):2580-2588. doi:10.7150/jca.24896
Long non-coding RNA CRYBG3 regulates glycolysis of lung cancer cells by interacting with lactate dehydrogenase A
1. School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou 215123, China
2. Collaborative Innovation Center of Radiological Medicine of Jiangsu Higher Education Institutions, Suzhou 215123, China
3. Medical College of Soochow University, Suzhou 215123, China
4. The Second Affiliated Hospital of Soochow University, Suzhou 215123, China
5. Center for Radiological Research, College of Physician and Surgeons, Columbia University, New York, NY 10032, USA
*These authors contributed equally.
Cancer cells usually utilize glucose as a carbon source for aerobic glycolysis, a phenomenon known as the Warburg effect. And a high rate of glycolysis has been observed in lung cancer cells. The growing evidence indicates that long non-coding RNAs (lncRNAs) are important players in lung cancer initiation and progression. However, the correlation between lncRNAs and glycolysis remains unclear. In this study, we recognized a lncRNA, LNC CRYBG3, which can interact with lactate dehydrogenase A (LDHA), a vital enzyme of glycolysis, is highly upregulated in both clinical lung cancer tissues and in vitro cultured lung cancer cell lines. A positive correlation between the expression level of LNC CRYBG3 and LDHA expression levels is observed. In another hand, LNC CRYBG3 is a regulator of glycolysis and its overexpression promoted the uptake of glucose and the production of lactate whereas the knockdown of LNC CRYBG3 led to opposite results and suppressed cell proliferation. These results indicated that LNC CRYBG3 might be a novel target for lung cancer treatment.
Keywords: LNC CRYBG3, LDHA, Glycolysis, Pyruvate, Lactate, Lung cancer
Chen H, Pei H, Hu W, Ma J, Zhang J, Mao W, Nie J, Xu C, Li B, Hei TK, Wang C, Zhou G. Long non-coding RNA CRYBG3 regulates glycolysis of lung cancer cells by interacting with lactate dehydrogenase A. J Cancer 2018; 9(14):2580-2588. doi:10.7150/jca.24896. Available from http://www.jcancer.org/v09p2580.htm