Abstract
The aim of the present study was to investigate the effects of transketolase (TKT) on cell proliferation, cell migration and interaction with other metabolism-associated genes in A549 lung cancer cells. A549 cells were transfected with three TKT-specific small interfering (si)RNAs, screened for the optimal transfection concentration, and sequenced with flow cytometry and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cell viability was evaluated using Cell Counting Kit-8 (CCK-8), cell cycle was assessed by flow cytometric analysis. Cell migration was determined by scratch-wound and Transwell chamber assays. The changes in mRNA expression levels of glucose-6-phosphate dehydrogenase (G6PDH), transaldolase (TAL), sorbitol dehydrogenase (SORD), phosphoribosyl pyrophosphate synthetase 1 (PRPS1) and hexokinase 1 (HK1) were detected by RT-qPCR. siRNA-C at 50 nmol/l was selected for the subsequent experiments. Compared with the negative control, cell proliferation of the TKT-siRNA-C group was inhibited dramatically (CCK-8 24 h, 0.2984±0.0371 vs. 0.0952±0.0063; P<0.0001), the cell cycle was arrested at the G1/G0 cell cycle phase (58±2.0% vs. 70±2.5%; P=0.002), and cell migration ability was decreased [wound size, 254.71±34.96 vs. 349.12±37.43 µm (P=0.0001); Transwell migration, 250±47.8/field vs. 150±49.0/field (P<0.0001)]. The mRNA expression levels of G6PDH, TAL, SORD, PRPS1 and HK1 were downregulated in the TKT-siRNA-C group compared with the negative control. The present study revealed that synthetic TKT-siRNA can inhibit A549 cell viability and migration, which may be due to arrest of the cell cycle and downregulation of relevant metabolic enzymes.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
