Objective:To investigate whether the nutrition support team (NST) benefits esophageal carcinoma (EC) patients who are concurrently undergoing chemoradiotherapy. Methods: Between June 2012 and December 2013, 40 EC patients undergoing chemoradiotherapy were divided into the NST group and routine treatment (RT) group, with 20 patients in each group. At the end of chemoradiotherapy, the nutritional status, incidence of complications, and completion rates of radiotherapy were evaluated. The length of hospital stay (LOS) and cost were also compared between the two groups. Results:The nutrition and blood parameter values of the NST group were better (P<0.05) than those of the RT group. The incidence of complications was lower in the NST group (P<0.05) than that in the RT group. In addition, all patients in the NST group achieved the treatment plan, whereas five of the patients in the RT group interrupted or delayed the plan (P<0.05). The average LOS decreased by 3.8 d (P<0.05), and the hospitalization costs were reduced to 6300 RMB person-times (P>0.05) for the patients of the NST group. Conclusion: NST could maintain the nutritional status and improve the treatment compliance and tolerance of EC patients undergoing chemoradiotherapy, thereby shortening the LOS time and reducing the costs.

Metabolic reprogramming is a hallmark of cancer, including lung cancer. However, the exact underlying mechanism and therapeutic potential are largely unknown. Here we report that protein arginine methyltransferase 6 (PRMT6) is highly expressed in lung cancer and is required for cell metabolism, tumorigenicity, and cisplatin response of lung cancer. PRMT6 regulated the oxidative pentose phosphate pathway (PPP) flux and glycolysis pathway in human lung cancer by increasing the activity of 6-phospho-gluconate dehydrogenase (6PGD) and α-enolase (ENO1). Furthermore, PRMT6 methylated R324 of 6PGD to enhancing its activity; while methylation at R9 and R372 of ENO1 promotes formation of active ENO1 dimers and 2-phosphoglycerate (2-PG) binding to ENO1, respectively. Lastly, targeting PRMT6 blocked the oxidative PPP flux, glycolysis pathway, and tumor growth, as well as enhanced the anti-tumor effects of cisplatin in lung cancer. Together, this study demonstrates that PRMT6 acts as a post-translational modification (PTM) regulator of glucose metabolism, which leads to the pathogenesis of lung cancer. It was proven that the PRMT6-6PGD/ENO1 regulatory axis is an important determinant of carcinogenesis and may become a promising cancer therapeutic strategy.