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Background Gastric cancer (GC) with hepatic metastasis has a poor prognosis. Understanding the molecular mechanisms involved in hepatic metastasis may contribute to the development of sensitive diagnostic biomarkers and novel therapeutic strategies. Methods We performed transcriptome analysis of surgically resected specimens from patients with advanced GC. One of the genes identified as specifically associated with hepatic metastasis was selected for detailed analysis. GC cell lines with knockout of the candidate gene were evaluated in vitro and in vivo. Expression of the candidate gene was analysed in GC tissues from 300 patients. Results Ethanolamine kinase 2 ( ETNK2 ) was differentially upregulated in GC patients with hepatic metastasis.  ETNK2  expression was elevated in GC cell lines derived from haematogenous metastases.  ETNK2  knockout significantly suppressed proliferation, invasion, and migration; increased apoptosis; reduced Bcl-2 protein expression; and increased phosphorylated p53 expression. In mouse xenograft models,  ETNK2  knockout virtually abolished hepatic metastasis. Stratification of GC patients based on  ETNK2  mRNA level revealed significant associations between high  ETNK2  tumour expression and both hepatic recurrence and worse prognosis. Conclusions Upregulation of  ETNK2  in GC enhances hepatic metastasis, possibly via dysregulation of p53 – Bcl-2 - associated apoptosis.  ETNK2  expression may serve as a biomarker for predicting hepatic recurrence and a therapeutic target.

Hepatic metastasis of gastric cancer is associated with enhanced expression of ethanolamine kinase 2 via the p53–Bcl-2 intrinsic apoptosis pathway