PLOD1 contributes to proliferation and glycolysis in hepatocellular carcinoma by regulating E2F1

Abstract

Purpose: To evaluate the effect of procollagen-lysine 1,2-oxoglutarate 5-dioxygenase 1 (PLOD1) in hepatocellular carcinoma (HCC). Methods: HCC cells were subjected to loss of function assays via transfection with siRNA targeting PLOD1. Colony formation and cell counting kit 8 (CCK8) were used to determine cell proliferation. Cell cycle was evaluated by flow cytometry while extracellular acidification rate (ECAR) levels, glucose consumption, and lactate production were determined to investigate aerobic glycolysis. Results: PLOD1 was significantly up-regulated in HCC tissues and cells compared to normal tissues and cells (p < 0.001). Silencing of PLOD1 significantly repressed cell proliferation (p < 0.001) and induced cell cycle arrest in HCC at the G1 phase. ECAR levels, glucose consumption, and lactate production in HCC were reduced by knockdown of PLOD1. Loss of PLOD1 down-regulated the expression of E2F1, while over-expression of E2F1 attenuated PLOD1 knockdown-induced decreases in cell viability, glucose consumption, and lactate production in HCC. Conclusion: Knockdown of PLOD1 inhibits cell proliferation and aerobic glycolysis in HCC via down-regulation of E2F1. Thus, PLOD1 may help in developing an effective strategy for the management of liver cancer.