Ge Cui1, Yuxuan Huang2, Wenming Feng3, Yunliang Yao4, Hongchang Zhou5, Xining Li6, Hui Gong7, Jun Liu8, Yifan Luo8, Yandi Sun9,10, Mengya Zhang9,10, Yan Luo9,10, Ting Zhang6. 1. Department of Pathology, The First Affiliated Hospital of Huzhou University, Huzhou, China. 2. School of Medicine, Huaqiao University, Quanzhou, Fujian, China. 3. Department of Surgery, The First Affiliated Hospital of Huzhou University, Huzhou, China. 4. Key Laboratory of Vector Biology and Pathogen Control of Zhejiang Province, Huzhou University, Huzhou Central Hospital, Huzhou, China. 5. Department of Pathogenic Biology, School of Medicine and Nursing Sciences, Huzhou University, Huzhou Central Hospital, Huzhou, China. 6. Department of Pathology, School of Medicine and Nursing Sciences, Huzhou University, Huzhou Central Hospital, Huzhou, China. 7. Central Laboratory, The First Affiliated Hospital of Huzhou University, Huzhou, China. 8. School of Medicine and Nursing Sciences, Huzhou University, Huzhou Central Hospital, Huzhou, China. 9. Department of Biochemistry and Cancer Institute of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China. 10. Key Laboratory of Cancer Prevention and Intervention of China National Ministry of Education, Hangzhou, China.
Abstract
BACKGROUND: Our study aims to investigate the effect of colon cancer-associated transcript-1 (CCAT-1) on colon cancer cells' activity and metabolism under different glucose environments in vitro and in vivo. METHODS: The levels of proliferation, migration, glucose, lactic acid, glucose metabolism-related enzymes, apoptosis genes, epithelial-mesenchymal transition (EMT) marker proteins, and PI3K/Akt/C-MYC pathway in CCAT-1-silenced SW620 cells cultured with different glucose levels were tested. Twenty BALB/C nude mice with hyperglycemia or normal blood sugar were transplanted with CCAT-1-silenced SW620 cells, blood glucose levels, lactic acid, insulin, and volume of transplanted tumor cells, the expression of EMT marker proteins, and PI3K/Akt/C-MYC pathway was detected. RESULTS: The levels of proliferation, migration, glucose, lactic acid, LDH-A, PKM2, and HK2 decreased, apoptosis increased in SW620 cells cultured with low glucose or silenced CCAT-1 (P<0.05); levels of E-cadherin and ZO-1 significantly increased, and levels of N-cadherin, vimentin, and p-Akt decreased in CCAT-1-silenced SW620 cells cultured with high glucose (P<0.05). Hyperglycemic nude mice transplanted with CCAT-1-silenced colon cancer cells showed decreased tumor volume, blood glucose, lactic acid, insulin, P-AKT, and P-C-MYC than EV group (P<0.05). CONCLUSIONS: CCAT-1 can enhance glucose metabolism and proliferation and migration of colon cancer cells by upregulating the expression of glycolysis enzymes, inhibiting apoptosis, activating the Akt/C-MYC pathway, and promoting EMT expression. 2020 Journal of Gastrointestinal Oncology. All rights reserved.
BACKGROUND: Our study aims to investigate the effect of colon cancer-associated transcript-1 (CCAT-1) on colon cancer cells' activity and metabolism under different glucose environments in vitro and in vivo. METHODS: The levels of proliferation, migration, glucose, lactic acid, glucose metabolism-related enzymes, apoptosis genes, epithelial-mesenchymal transition (EMT) marker proteins, and PI3K/Akt/C-MYC pathway in CCAT-1-silenced SW620 cells cultured with different glucose levels were tested. Twenty BALB/C nude mice with hyperglycemia or normal blood sugar were transplanted with CCAT-1-silenced SW620 cells, blood glucose levels, lactic acid, insulin, and volume of transplanted tumor cells, the expression of EMT marker proteins, and PI3K/Akt/C-MYC pathway was detected. RESULTS: The levels of proliferation, migration, glucose, lactic acid, LDH-A, PKM2, and HK2 decreased, apoptosis increased in SW620 cells cultured with low glucose or silenced CCAT-1 (P<0.05); levels of E-cadherin and ZO-1 significantly increased, and levels of N-cadherin, vimentin, and p-Akt decreased in CCAT-1-silenced SW620 cells cultured with high glucose (P<0.05). Hyperglycemic nude mice transplanted with CCAT-1-silenced colon cancer cells showed decreased tumor volume, blood glucose, lactic acid, insulin, P-AKT, and P-C-MYC than EV group (P<0.05). CONCLUSIONS: CCAT-1 can enhance glucose metabolism and proliferation and migration of colon cancer cells by upregulating the expression of glycolysis enzymes, inhibiting apoptosis, activating the Akt/C-MYC pathway, and promoting EMT expression. 2020 Journal of Gastrointestinal Oncology. All rights reserved.
Authors: Yanan Ma; Wanshui Yang; Mingyang Song; Stephanie A Smith-Warner; Juhong Yang; Yanping Li; Wenjie Ma; Yang Hu; Shuji Ogino; Frank B Hu; Deliang Wen; Andrew T Chan; Edward L Giovannucci; Xuehong Zhang Journal: Br J Cancer Date: 2018-11-07 Impact factor: 7.640
Authors: Jetty A Overbeek; Josephina G Kuiper; Amber A W A van der Heijden; Mariette Labots; Ulrike Haug; Ron M C Herings; Giel Nijpels Journal: Int J Colorectal Dis Date: 2018-11-12 Impact factor: 2.571
Authors: Sander de Kort; Colinda C J M Simons; Piet A van den Brandt; Maryska L G Janssen-Heijnen; Silvia Sanduleanu; Ad A M Masclee; Matty P Weijenberg Journal: Int J Cancer Date: 2019-05-06 Impact factor: 7.396