It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
As an important component of the tumor microenvironment, cancer-associated fibroblasts (CAFs) secrete energy metabolites to supply energy for tumor progression. Abnormal regulation of long noncoding RNAs (lncRNAs) is thought to contribute to glucose metabolism, but the role of lncRNAs in glycolysis in oral CAFs has not been systematically examined. In the present study, by using RNA sequencing and bioinformatics analysis, we analyzed the lncRNA/mRNA profiles of normal fibroblasts (NFs) derived from normal tissues and CAFs derived from patients with oral squamous cell carcinoma (OSCC). LncRNA H19 was identified as a key lncRNA in oral CAFs and was synchronously upregulated in both oral cancer cell lines and CAFs. Using small interfering RNA (siRNA) strategies, we determined that lncRNA H19 knockdown affected proliferation, migration, and glycolysis in oral CAFs. We found that knockdown of lncRNA H19 by siRNA suppressed the MAPK signaling pathway, 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3) and miR-675-5p. Furthermore, the lncRNA H19/miR-675-5p/PFKFB3 axis was involved in promoting the glycolysis pathway in oral CAFs, as demonstrated by a luciferase reporter system assay and treatment with a miRNA-specific inhibitor. Our study presents a new way to understand glucose metabolism in oral CAFs, theoretically providing a novel biomarker for OSCC molecular diagnosis and a new target for antitumor therapy.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 Sichuan University, State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & National Center of Stomatology, West China Hospital of Stomatology, Chengdu, China (GRID:grid.13291.38) (ISNI:0000 0001 0807 1581)
2 Sichuan University, Department of Oral and Maxillofacial Surgery, West China Hospital of Stomatology, Chengdu, China (GRID:grid.13291.38) (ISNI:0000 0001 0807 1581)
3 Sichuan University, State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & National Center of Stomatology, West China Hospital of Stomatology, Chengdu, China (GRID:grid.13291.38) (ISNI:0000 0001 0807 1581); Zhejiang University, Department of Oral Medicine, the Second Affiliated Hospital, School of Medicine, Hangzhou, China (GRID:grid.13402.34) (ISNI:0000 0004 1759 700X)
4 Sichuan University, State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & National Center of Stomatology, West China Hospital of Stomatology, Chengdu, China (GRID:grid.13291.38) (ISNI:0000 0001 0807 1581); Zhejiang University, Department of General Dentistry, the Second Affiliated Hospital, School of Medicine, Hangzhou, China (GRID:grid.13402.34) (ISNI:0000 0004 1759 700X)