Correction: C-terminal truncated HBx initiates hepatocarcinogenesis by downregulating TXNIP and reprogramming glucose metabolism

Correction to: Oncogene 10.1038/s41388-020-01593-5, published online 15 December 2020

Unfortunately, an error occurred in Fig. 5 and in legend to Fig. 5.

Fig. 5. TXNIP induced glucose metabolism reprogramming from glycolysis to mitochondrial respiration.

A Schematic representation of the biological process of glucose metabolism in normal cells and cancer cells. B Heatmap showing the relative expression level of several genes involved in glucose metabolism in Ct-HBx and vectors containing samples as indicated by RNA sequencing, each matrix representing the relative expression level of an individual gene; high and low expressions are indicated by yellow and blue color. C The expression level of the gene panel indicated above was validated by qRT-PCR in MIHA cells transduced with truncated HBx mutants compared with the vector group; also, the expression was further compared after re-introduction of TXNIP into Ct-HBx-expressing cells. D Re-introduction of TXNIP into Ct-HBx- (HBx-120, HBx-134) expressing cells was confirmed at the protein and genomic level by western blotting and qRT-PCR. E The expression level of several key enzymes and molecules that participated in glycolysis and Krebs cycle are determined by western blotting. The expression of internal reference β-actin can be referred to in (D). F Level of glucose uptake, lactate secretion, and relative ATP production activity was compared among vector, Ct-HBx as well as TXNIP overexpression samples. G The activation of the mTOR-HIF1α axis was detected by western blotting; β-actin was used as an internal reference. H Analysis of cell distribution in each stage of the cell cycle in each transfected MIHA cell.

The corrected Fig. 5 with the corrected legend is given below.

The original article has been corrected.