Mounting evidence indicates the potential involvement of
ATP-citrate lyase (ACLY) in the modulation of various
cancer types. Nevertheless, the precise
biological significance of ACLY in
gastric cancer (GC) remains elusive. This study sought to elucidate the
biological function of ACLY and uncover its influence on peritoneal
metastasis in GC. The expression of ACLY was assessed using both real-time quantitative PCR and western blot techniques. To investigate the impact of ACLY on the proliferation of
gastric cancer (GC) cells, colony formation and
5-ethynyl-2'-deoxyuridine (EdU) assays were performed. The migratory and invasive abilities of GC were evaluated using wound healing and transwell assays. Additionally, a bioinformatics analysis was employed to predict the correlation between ACLY and HIF-1A. This interaction was subsequently confirmed through a
chromatin immunoprecipitation (ChIP) assay. ACLY exhibited upregulation in
gastric cancer (GC) as well as in peritoneal
metastasis. Its overexpression was found to facilitate the proliferation and
metastasis of GC cells in both in vitro and in vivo experiments. Moreover, ACLY was observed to play a role in promoting angiogenesis and epithelial-mesenchymal transition (EMT). Notably, under hypoxic conditions, HIF-1A levels were elevated, thereby acting as a
transcription factor to upregulate ACLY expression. Under the regulatory influence of HIF-1A, ACLY exerts a significant impact on the progression of
gastric cancer, thereby facilitating peritoneal
metastasis.