GLUT1 and PKM2 may be useful prognostic predictors in patients with non‑small cell lung cancer following curative R0 resection

Oncol Lett. 2023 Feb 10;25(3):129. doi: 10.3892/ol.2023.13715. eCollection 2023 Mar.

Abstract

Lung cancer has a poor prognosis despite recent progresses being made regarding its treatment. In addition, there is a paucity of reliable and independent prognostic predictors for non-small cell lung cancer (NSCLC) following curative resection. Glycolysis is associated with the malignancy and proliferation of cancer cells. Glucose transporter 1 (GLUT1) promotes glucose uptake, whereas pyruvate kinase M2 (PKM2) promotes anaerobic glycolysis. The present study aimed to evaluate the relationship between the expression of GLUT1 and PKM2 and the clinicopathological features of patients with NSCLC, and to identify a reliable prognostic factor for NSCLC following curative resection. Patients with NSCLC who underwent curative surgery were retrospectively enrolled to the present study. GLUT1 and PKM2 expression was assessed using immunohistochemistry. Subsequently, the association between the clinicopathological features of patients with NSCLC and the expression of GLUT1 and PKM2 was assessed. Of the 445 patients with NSCLC included in the present study, 65 (15%) were positive for both GLUT1 and PKM2 expression (G+/P+ group). GLUT1 and PKM2 positivity was significantly associated with sex, absence of adenocarcinoma, lymphatic invasion and pleural invasion. Furthermore, patients with NSCLC in the G+/P+ group presented significantly poorer survival rates than those expressing other markers. G+/P+ expression was significantly associated with poor disease-free survival. In conclusion, the findings of the present study indicated that the combination of GLUT1 and PKM2 may be considered a reliable prognostic factor for patients with NSCLC following curative resection, especially in patients with stage I NSCLC.

Keywords: curative resection; glucose transporter 1; non-small cell lung cancer; predictive marker; pyruvate kinase M2.

Grants and funding

This study was supported by KAKENHI (Grants-in-Aid for Scientific Research, grant no. 21H03008) by the Japan Society for the Promotion of Science.