Lihui Zhu1,2,3, Ruzhen Jia2, Junyong Zhang2, Xiao Li2, Chengyong Qin2, Qi Zhao2. 1. Department of Gastroenterology, Shandong Provincial Hospital affiliated to Shandong University, Jinan, 250021, P. R. China. 2. Department of Gastroenterology, Shandong Provincial Hospital affiliated to Shandong First Medical University, Jinan, 250021, P. R. China. 3. Shandong Provincial Engineering and Technological Research Center for Liver Diseases Prevention and Control, Jinan, 250021, P. R. China.
Abstract
PURPOSE: The molecular pathogenesis of gastric cancer is still ambiguous till now. Here, it is demonstrated that long noncoding RNA (lncRNA) Ftx acts as a novel tumor promotor of gastric cancer and a potent regulator of hexokinase-2 (HK2). EXPERIMENTAL DESIGN: The role of lncRNA Ftx is detected in the loss and gain-of-function models of gastric cancer cells. Tandem mass tags combined with multidimensional LC and MS analyses are performed to decipher comparative proteomic profiles of gastric cancer cells in response to lncRNA Ftx knockdown and overexpression. Real-time roteomics-clinical applications (PCR) and western blot are used to validate the proteomic data. RESULTS: A total of 5124 proteins are quantified and indicated in diverse biological functions and metabolic related signaling pathways. Interestingly, HK2, which is downregulated when lncRNA Ftx is deleted and upregulated while lncRNA Ftx is overexpressed, is further validated in gastric cancer cells. CONCLUSIONS AND CLINICAL RELEVANCE: The present study suggests lncRNA Ftx promotes gastric cancer progression by upregulating HK2, which provides a new perspective for the mechanism of gastric cancer progression, and thus identifies potential therapeutic targets for gastric cancer.
PURPOSE: The molecular pathogenesis of gastric cancer is still ambiguous till now. Here, it is demonstrated that long noncoding RNA (lncRNA) Ftx acts as a novel tumor promotor of gastric cancer and a potent regulator of hexokinase-2 (HK2). EXPERIMENTAL DESIGN: The role of lncRNA Ftx is detected in the loss and gain-of-function models of gastric cancer cells. Tandem mass tags combined with multidimensional LC and MS analyses are performed to decipher comparative proteomic profiles of gastric cancer cells in response to lncRNA Ftx knockdown and overexpression. Real-time roteomics-clinical applications (PCR) and western blot are used to validate the proteomic data. RESULTS: A total of 5124 proteins are quantified and indicated in diverse biological functions and metabolic related signaling pathways. Interestingly, HK2, which is downregulated when lncRNA Ftx is deleted and upregulated while lncRNA Ftx is overexpressed, is further validated in gastric cancer cells. CONCLUSIONS AND CLINICAL RELEVANCE: The present study suggests lncRNA Ftx promotes gastric cancer progression by upregulating HK2, which provides a new perspective for the mechanism of gastric cancer progression, and thus identifies potential therapeutic targets for gastric cancer.