Protein kinase C-iota-mediated glycolysis promotes non-small-cell lung cancer progression

• Published in: OncoTargets and therapy 2019-07, Vol.12, p.5835-5848
• Main Authors: Liu, Liu, Lei, Bei, Wang, Lihua, Chang, Cheng, Yang, Hao, Liu, Jianjun, Huang, Gang, Xie, Wenhui
• Format: Article
• Language: English
• Subjects: CAT scans; Glucose; Glucose metabolism; Lung cancer; Non-small cell lung cancer; Original Research; Physiological aspects; Positron emission tomography; Protein kinases; Surgery; Tomography; Tumor removal; Tumors
• ISSN: 1178-6930; 1178-6930
• DOI: 10.2147/ott.s207211

To determine whether protein kinase C-iota (PKC-iota) is associated with glucose metabolism in non-small-cell lung cancer (NSCLC) and whether its regulatory effect on metabolic and biological changes observed in NSCLC can be mediated by glucose transporter 1 (GLUT1). Forty-five NSCLC patients underwent combined F-fludeoxyglucose ( F-FDG) positron emission tomography and computed tomography (PET/CT) before surgery, and another eighty-one NSCLC patients were followed-up for 1-91 months after tumor resection. The rate of glucose metabolism in NSCLC was quantified by measuring the maximum standardized uptake value (SUVmax) by F-FDG PET/CT. PKC-iota and GLUT1 in NSCLC were detected by immunostaining. In vitro, PKC-iota was knocked down, whereas GLUT1 was silenced with or without PKC-iota overexpression to identify the role of PKC-iota in glycolysis. Spearman's rank correlation coefficient was used in the correlation analysis. Kaplan-Meier analysis was used to assess survival duration. There was a positive relationship between PKC-iota expression and SUVmax in NSCLC (r=0.649,